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154. Functional characterization of the Sjögren's syndrome-associated locus DDX6-CXCR5

Author

Khanam, Sharmily, Joachims, Michelle L., Means, Nicholas, Adrianto, Indra, Rasmussen, Astrid, Bowman, Simon J., Lewis, David M., Radfar, Lida, Omdal, Roald, Wahren-Herleniuss, Marie, Alevizos, Ilias, Witte, Torsten, Jonsson, Roland, Rischmueller, Maureen, Gaffney, Patrick M., James, Judith A., Rönnblom, Lars, Theander, Elke, Rhodus, Nelson L., Segal, Barbara M., Scofield, R. Hal, Montgomery, Courtney G., Mariette, Xavier, Ng, Wan-Fai, Nordmark, Gunnel, Sivils, Kathy L., Lessard, Christopher J., Khanam, Sharmily, Joachims, Michelle L., Means, Nicholas, Adrianto, Indra, Rasmussen, Astrid, Bowman, Simon J., Lewis, David M., Radfar, Lida, Omdal, Roald, Wahren-Herleniuss, Marie, Alevizos, Ilias, Witte, Torsten, Jonsson, Roland, Rischmueller, Maureen, Gaffney, Patrick M., James, Judith A., Rönnblom, Lars, Theander, Elke, Rhodus, Nelson L., Segal, Barbara M., Scofield, R. Hal, Montgomery, Courtney G., Mariette, Xavier, Ng, Wan-Fai, Nordmark, Gunnel, Sivils, Kathy L., and Lessard, Christopher J.

Published
2018

155. Genetic basis and clinical evidence for two variants of primary Sjögren's syndrome with distinct outcomes

Author

Thorlacius, Gudny Ella, Hultin-Rosenberg, Lina, Sandling, Johanna K., Imgenberg-Kreuz, Juliana, Theander, Elke, Kvarnstrom, Marika, Forsblad-d'Elia, Helena, Bucher, Sara Magnusson, Norheim, Katrine Braekke, Johnsen, Svein Joar, Hammenfors, Daniel, Skarstein, Kathrine, Jonsson, Malin V., Baecklund, Eva, Mandl, Thomas, Eriksson, Per, Omdal, Roald, Jonsson, Roland, Lindblad-Toh, Kerstin, Rönnblom, Lars, Wahren-Herlenius, Marie, Nordmark, Gunnel, Thorlacius, Gudny Ella, Hultin-Rosenberg, Lina, Sandling, Johanna K., Imgenberg-Kreuz, Juliana, Theander, Elke, Kvarnstrom, Marika, Forsblad-d'Elia, Helena, Bucher, Sara Magnusson, Norheim, Katrine Braekke, Johnsen, Svein Joar, Hammenfors, Daniel, Skarstein, Kathrine, Jonsson, Malin V., Baecklund, Eva, Mandl, Thomas, Eriksson, Per, Omdal, Roald, Jonsson, Roland, Lindblad-Toh, Kerstin, Rönnblom, Lars, Wahren-Herlenius, Marie, and Nordmark, Gunnel

Published
2018

156. Correction: Klinefelters syndrome (47,XXY) is in excess among men with Sjogrens syndrome (vol 168, pg 25, 2016)

Author

Harris, Valerie M., Sharma, Rohan, Cavett, Joshua, Kurien, Biji T., Liu, Ke, Koelsch, Kristi A., Rasmussen, Astrid, Radfar, Lida, Lewis, David, Stone, Donald U., Kaufman, C. Erick, Li, Shibo, Segal, Barbara, Wallace, Daniel J., Weisman, Michael H., Venuturupalli, Swamy, Kelly, Jennifer A., Alarcon-Riquelme, Marta E., Pons-Estel, Bernardo, Jonsson, Roland, Lu, Xianglan, Gottenberg, Jacques-Eric, Anaya, Juan-Manuel, Cunninghame-Graham, Deborah S., Huang, Andrew J. W., Brennan, Michael T., Hughes, Pamela, Alevizos, Ilias, Miceli-Richard, Corinne, Keystone, Edward C., Bykerk, Vivian P., Hirschfield, Gideon, Xie, Gang, Siminovitch, Katherine A., Ng, Wan-Fai, Nordmark, Gunnel, Bucher, Sara Magnusson, Eriksson, Per, Omdal, Roald, Rhodus, Nelson L., Rischmueller, Maureen, Rohrer, Michael, Wahren-Herlenius, Marie, Witte, Torsten, Mariette, Xavier, Lessard, Christopher J., Harley, John B., Sivils, Kathy L., Scofield, R. Hal, Harris, Valerie M., Sharma, Rohan, Cavett, Joshua, Kurien, Biji T., Liu, Ke, Koelsch, Kristi A., Rasmussen, Astrid, Radfar, Lida, Lewis, David, Stone, Donald U., Kaufman, C. Erick, Li, Shibo, Segal, Barbara, Wallace, Daniel J., Weisman, Michael H., Venuturupalli, Swamy, Kelly, Jennifer A., Alarcon-Riquelme, Marta E., Pons-Estel, Bernardo, Jonsson, Roland, Lu, Xianglan, Gottenberg, Jacques-Eric, Anaya, Juan-Manuel, Cunninghame-Graham, Deborah S., Huang, Andrew J. W., Brennan, Michael T., Hughes, Pamela, Alevizos, Ilias, Miceli-Richard, Corinne, Keystone, Edward C., Bykerk, Vivian P., Hirschfield, Gideon, Xie, Gang, Siminovitch, Katherine A., Ng, Wan-Fai, Nordmark, Gunnel, Bucher, Sara Magnusson, Eriksson, Per, Omdal, Roald, Rhodus, Nelson L., Rischmueller, Maureen, Rohrer, Michael, Wahren-Herlenius, Marie, Witte, Torsten, Mariette, Xavier, Lessard, Christopher J., Harley, John B., Sivils, Kathy L., and Scofield, R. Hal

Abstract

n/a, Funding Agencies|BLRD VA [I01 BX001451]

Published
2018
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160. X Chromosome Dose and Sex Bias in Autoimmune Diseases:Increased Prevalence of 47,XXX in Systemic Lupus Erythematosus and Sjögren's Syndrome

Author

Liu, Ke, Kurien, Biji T, Zimmerman, Sarah L, Kaufman, Kenneth M, Taft, Diana H, Kottyan, Leah C, Lazaro, Sara, Weaver, Carrie A, Ice, John A, Adler, Adam J, Chodosh, James, Radfar, Lida, Rasmussen, Astrid, Stone, Donald U, Lewis, David M, Li, Shibo, Koelsch, Kristi A, Igoe, Ann, Talsania, Mitali, Kumar, Jay, Maier-Moore, Jacen S, Harris, Valerie M, Gopalakrishnan, Rajaram, Jonsson, Roland, Lessard, James A, Lu, Xianglan, Gottenberg, Jacques-Eric, Anaya, Juan-Manuel, Cunninghame-Graham, Deborah S, Huang, Andrew J W, Brennan, Michael T, Hughes, Pamela, Illei, Gabor G, Miceli-Richard, Corinne, Keystone, Edward C, Bykerk, Vivian P, Hirschfield, Gideon, Xie, Gang, Ng, Wan-Fai, Nordmark, Gunnel, Eriksson, Per, Omdal, Roald, Rhodus, Nelson L, Rischmueller, Maureen, Rohrer, Michael, Segal, Barbara M, Vyse, Timothy J, Wahren-Herlenius, Marie, Witte, Torsten, Pons-Estel, Bernardo, Alarcon-Riquelme, Marta E, Guthridge, Joel M, James, Judith A, Lessard, Christopher J, Kelly, Jennifer A, Thompson, Susan D, Gaffney, Patrick M, Montgomery, Courtney G, Edberg, Jeffrey C, Kimberly, Robert P, Alarcón, Graciela S, Langefeld, Carl L, Gilkeson, Gary S, Kamen, Diane L, Tsao, Betty P, McCune, W Joseph, Salmon, Jane E, Merrill, Joan T, Weisman, Michael H, Wallace, Daniel J, Utset, Tammy O, Bottinger, Erwin P, Amos, Christopher I, Siminovitch, Katherine A, Mariette, Xavier, Sivils, Kathy L, Harley, John B, and Scofield, R Hal

Subjects
Gene dosage, Liver Cirrhosis, Sarcoidosis, Sex Chromosome Disorders of Sex Development, Case control study, Trisomy, Major clinical study, XXX, Article, Fluorescence, Chromosomes, Autoimmune Diseases, X chromosome, Systemic lupus erythematosus, Rheumatoid, Autoimmune disease, Prevalence, Live birth, Humans, Rheumatoid arthritis, Sex Distribution, Sex Chromosome Aberrations, In Situ Hybridization, Priority journal, Lupus Erythematosus, Fluorescence in situ hybridization, Arthritis, Systemic, Biliary, Quality control, Polymerase chain reaction, Single nucleotide polymorphism, Sjogren's Syndrome, Primary biliary cirrhosis, Sex chromosome aberration, Case-Control Studies, Female, Sex, Karyotype 47, Controlled study, Sex ratio, Human
Abstract

Objective More than 80% of autoimmune disease predominantly affects females, but the mechanism for this female bias is poorly understood. We suspected that an X chromosome dose effect accounts for this, and we undertook this study to test our hypothesis that trisomy X (47,XXX; occurring in ?1 in 1,000 live female births) would be increased in patients with female-predominant diseases (systemic lupus erythematosus [SLE], primary Sjögren's syndrome [SS], primary biliary cirrhosis, and rheumatoid arthritis [RA]) compared to patients with diseases without female predominance (sarcoidosis) and compared to controls. Methods All subjects in this study were female. We identified subjects with 47,XXX using aggregate data from single-nucleotide polymorphism arrays, and, when possible, we confirmed the presence of 47,XXX using fluorescence in situ hybridization or quantitative polymerase chain reaction. Results We found 47,XXX in 7 of 2,826 SLE patients and in 3 of 1,033 SS patients, but in only 2 of 7,074 controls (odds ratio in the SLE and primary SS groups 8.78 [95% confidence interval 1.67-86.79], P = 0.003 and odds ratio 10.29 [95% confidence interval 1.18-123.47], P = 0.02, respectively). One in 404 women with SLE and 1 in 344 women with SS had 47,XXX. There was an excess of 47,XXX among SLE and SS patients. Conclusion The estimated prevalence of SLE and SS in women with 47,XXX was ?2.5 and ?2.9 times higher, respectively, than that in women with 46,XX and ?25 and ?41 times higher, respectively, than that in men with 46,XY. No statistically significant increase of 47,XXX was observed in other female-biased diseases (primary biliary cirrhosis or RA), supporting the idea of multiple pathways to sex bias in autoimmunity. © 2016, American College of Rheumatology.

Published
2016
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161. Corrigendum to “Klinefelter's syndrome (47,XXY) is in excess among men with Sjögren's syndrome” [Clin. Immunol. 168 (2016) 25–29]

Author

Harris, Valerie M., primary, Sharma, Rohan, additional, Cavett, Joshua, additional, Kurien, Biji T., additional, Liu, Ke, additional, Koelsch, Kristi A., additional, Rasmussen, Astrid, additional, Radfar, Lida, additional, Lewis, David, additional, Stone, Donald U., additional, Kaufman, C. Erick, additional, Li, Shibo, additional, Segal, Barbara, additional, Wallace, Daniel J., additional, Weisman, Michael H., additional, Venuturupalli, Swamy, additional, Kelly, Jennifer A., additional, Alarcon-Riquelme, Marta E., additional, Pons-Estel, Bernardo, additional, Jonsson, Roland, additional, Lu, Xianglan, additional, Gottenberg, Jacques-Eric, additional, Anaya, Juan-Manuel, additional, Cunninghame-Graham, Deborah S., additional, Huang, Andrew J.W., additional, Brennan, Michael T., additional, Hughes, Pamela, additional, Alevizos, Ilias, additional, Miceli-Richard, Corinne, additional, Keystone, Edward C., additional, Bykerk, Vivian P., additional, Hirschfield, Gideon, additional, Xie, Gang, additional, Siminovitch, Katherine A., additional, Ng, Wan-Fai, additional, Nordmark, Gunnel, additional, Bucher, Sara Magnusson, additional, Eriksson, Per, additional, Omdal, Roald, additional, Rhodus, Nelson L., additional, Rischmueller, Maureen, additional, Rohrer, Michael, additional, Wahren-Herlenius, Marie, additional, Witte, Torsten, additional, Mariette, Xavier, additional, Lessard, Christopher J., additional, Harley, John B., additional, Sivils, Kathy L., additional, and Scofield, R. Hal, additional

Published
2018
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162. Oral microbiota in autoimmune polyendocrine syndrome type 1

Author

Bruserud, Øyvind, primary, Siddiqui, Huma, additional, Marthinussen, Mihaela Cuida, additional, Chen, Tsute, additional, Jonsson, Roland, additional, Oftedal, Bergithe Eikeland, additional, Olsen, Ingar, additional, Husebye, Eystein Sverre, additional, and Wolff, Anette Bøe, additional

Published
2018
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163. Brief Report: Rare X Chromosome Abnormalities in Systemic Lupus Erythematosus and Sjögren's Syndrome

Author

Sharma, Rohan, primary, Harris, Valerie M., additional, Cavett, Joshua, additional, Kurien, Biji T., additional, Liu, Ke, additional, Koelsch, Kristi A., additional, Fayaaz, Anum, additional, Chaudhari, Kaustubh S., additional, Radfar, Lida, additional, Lewis, David, additional, Stone, Donald U., additional, Kaufman, C. Erick, additional, Li, Shibo, additional, Segal, Barbara, additional, Wallace, Daniel J., additional, Weisman, Michael H., additional, Venuturupalli, Swamy, additional, Kelly, Jennifer A., additional, Pons‐Estel, Bernardo, additional, Jonsson, Roland, additional, Lu, Xianglan, additional, Gottenberg, Jacques‐Eric, additional, Anaya, Juan‐Manuel, additional, Cunninghame‐Graham, Deborah S., additional, Huang, Andrew J. W., additional, Brennan, Michael T., additional, Hughes, Pamela, additional, Alevizos, Ilias, additional, Miceli‐Richard, Corinne, additional, Keystone, Edward C., additional, Bykerk, Vivian P., additional, Hirschfield, Gideon, additional, Nordmark, Gunnel, additional, Bucher, Sara Magnusson, additional, Eriksson, Per, additional, Omdal, Roald, additional, Rhodus, Nelson L., additional, Rischmueller, Maureen, additional, Rohrer, Michael, additional, Wahren‐Herlenius, Marie, additional, Witte, Torsten, additional, Alarcón‐Riquelme, Marta, additional, Mariette, Xavier, additional, Lessard, Christopher J., additional, Harley, John B., additional, Ng, Wan‐Fai, additional, Rasmussen, Astrid, additional, Sivils, Kathy L., additional, and Scofield, R. Hal, additional

Published
2017
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164. H1N1 vaccination in Sjögren’s syndrome triggers polyclonal B cell activation and promotes autoantibody production

Author

Brauner, Susanna, primary, Folkersen, Lasse, additional, Kvarnström, Marika, additional, Meisgen, Sabrina, additional, Petersen, Sven, additional, Franzén-Malmros, Michaela, additional, Mofors, Johannes, additional, Brokstad, Karl A, additional, Klareskog, Lars, additional, Jonsson, Roland, additional, Westerberg, Lisa S, additional, Trollmo, Christina, additional, Malmström, Vivianne, additional, Ambrosi, Aurelie, additional, Kuchroo, Vijay K, additional, Nordmark, Gunnel, additional, and Wahren-Herlenius, Marie, additional

Published
2017
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169. Standardisation of labial salivary gland histopathology in clinical trials in primary Sjögren's syndrome

Author

UMC Utrecht, Translationele immunologie, Infection & Immunity, Fisher, Benjamin A., Jonsson, Roland, Daniels, Troy, Bombardieri, Michele, Brown, Rachel M., Morgan, Peter, Bombardieri, Stefano, Ng, Wan Fai, Tzioufas, Athanasios G., Vitali, Claudio, Shirlaw, Pepe, Haacke, Erlin, Costa, Sebastian, Bootsma, Hendrika, Devauchelle-Pensec, Valerie, Radstake, Timothy R., Mariette, Xavier, Richards, Andrea, Stack, Rebecca, Bowman, Simon J., Barone, Francesca, UMC Utrecht, Translationele immunologie, Infection & Immunity, Fisher, Benjamin A., Jonsson, Roland, Daniels, Troy, Bombardieri, Michele, Brown, Rachel M., Morgan, Peter, Bombardieri, Stefano, Ng, Wan Fai, Tzioufas, Athanasios G., Vitali, Claudio, Shirlaw, Pepe, Haacke, Erlin, Costa, Sebastian, Bootsma, Hendrika, Devauchelle-Pensec, Valerie, Radstake, Timothy R., Mariette, Xavier, Richards, Andrea, Stack, Rebecca, Bowman, Simon J., and Barone, Francesca

Published
2017

170. Difference in Clinical Presentation between Female and Male Patients with Primary Sjogren's Syndrome at Diagnosis and in Long-Term Follow-up

Author

Ramirez, Jorge, Kvarnstrom, Marika, Brauner, Susanna, Baldini, Chiara, Eriksson, Per, Mandl, Thomas, Norheim, Katrine Braekke, Johnsen, Svein Joar, Hammenfors, Daniel S., Jonsson, Malin V., Skarstein, Kathrine, Brun, Johan G., Rönnblom, Lars, D'Elia, Helena Forsblad, Bucher, Sara Magnusson, Theander, Elke, Omdal, Roald, Jonsson, Roland, Nordmark, Gunnel, Wahren-Herlenius, Marie, Ramirez, Jorge, Kvarnstrom, Marika, Brauner, Susanna, Baldini, Chiara, Eriksson, Per, Mandl, Thomas, Norheim, Katrine Braekke, Johnsen, Svein Joar, Hammenfors, Daniel S., Jonsson, Malin V., Skarstein, Kathrine, Brun, Johan G., Rönnblom, Lars, D'Elia, Helena Forsblad, Bucher, Sara Magnusson, Theander, Elke, Omdal, Roald, Jonsson, Roland, Nordmark, Gunnel, and Wahren-Herlenius, Marie

Published
2017

171. Genetic Determinants of Fatigue in Primary Sjogren's Syndrome : a Genome Wide Association Study

Author

Norheim, Katrine, Alexsson, Andrei, Imgenberg-Kreuz, Juliana, Brun, Johan Gorgas, Jonsson, Roland, Ng, Wan-Fai, Theander, Elke, Mandl, Thomas, Sivils, Kathy L., Rönnblom, Lars, Nordmark, Gunnel, Omdal, Roald, Norheim, Katrine, Alexsson, Andrei, Imgenberg-Kreuz, Juliana, Brun, Johan Gorgas, Jonsson, Roland, Ng, Wan-Fai, Theander, Elke, Mandl, Thomas, Sivils, Kathy L., Rönnblom, Lars, Nordmark, Gunnel, and Omdal, Roald

Published
2017

172. Rare X Chromosome Abnormalities in Systemic Lupus Erythematosus and Sjögren's Syndrome

Author

Sharma, Rohan, Harris, Valerie M., Cavett, Joshua, Kurien, Biji T., Liu, Ke, Koelsch, Kristi A., Fayaaz, Anum, Chaudhari, Kaustubh S., Radfar, Lida, Lewis, David, Stone, Donald U., Kaufman, C. Erick, Li, Shibo, Segal, Barbara, Wallace, Daniel J., Weisman, Michael H., Venuturupalli, Swamy, Kelly, Jennifer A., Pons-Estel, Bernardo, Jonsson, Roland, Lu, Xianglan, Gottenberg, Jacques-Eric, Anaya, Juan-Manuel, Cunninghame-Graham, Deborah S., Huang, Andrew J. W., Brennan, Michael T., Hughes, Pamela, Alevizos, Ilias, Miceli-Richard, Corinne, Keystone, Edward C., Bykerk, Vivian P., Hirschfield, Gideon, Nordmark, Gunnel, Bucher, Sara Magnusson, Eriksson, Per, Omdal, Roald, Rhodus, Nelson L., Rischmueller, Maureen, Rohrer, Michael, Wahren-Herlenius, Marie, Witte, Torsten, Alarcon-Riquelme, Marta, Mariette, Xavier, Lessard, Christopher J., Harley, John B., Ng, Wan-Fai, Rasmussen, Astrid, Sivils, Kathy L., Scofield, R. Hal, Sharma, Rohan, Harris, Valerie M., Cavett, Joshua, Kurien, Biji T., Liu, Ke, Koelsch, Kristi A., Fayaaz, Anum, Chaudhari, Kaustubh S., Radfar, Lida, Lewis, David, Stone, Donald U., Kaufman, C. Erick, Li, Shibo, Segal, Barbara, Wallace, Daniel J., Weisman, Michael H., Venuturupalli, Swamy, Kelly, Jennifer A., Pons-Estel, Bernardo, Jonsson, Roland, Lu, Xianglan, Gottenberg, Jacques-Eric, Anaya, Juan-Manuel, Cunninghame-Graham, Deborah S., Huang, Andrew J. W., Brennan, Michael T., Hughes, Pamela, Alevizos, Ilias, Miceli-Richard, Corinne, Keystone, Edward C., Bykerk, Vivian P., Hirschfield, Gideon, Nordmark, Gunnel, Bucher, Sara Magnusson, Eriksson, Per, Omdal, Roald, Rhodus, Nelson L., Rischmueller, Maureen, Rohrer, Michael, Wahren-Herlenius, Marie, Witte, Torsten, Alarcon-Riquelme, Marta, Mariette, Xavier, Lessard, Christopher J., Harley, John B., Ng, Wan-Fai, Rasmussen, Astrid, Sivils, Kathy L., and Scofield, R. Hal

Abstract

Objective: Sjögren's syndrome (SS) and systemic lupus erythematosus (SLE) are related by clinical and serologic manifestations as well as genetic risks. Both diseases are more commonly found in women than in men, at a ratio of similar to 10 to 1. Common X chromosome aneuploidies, 47,XXY and 47,XXX, are enriched among men and women, respectively, in either disease, suggesting a dose effect on the X chromosome. Methods: We examined cohorts of SS and SLE patients by constructing intensity plots of X chromosome single-nucleotide polymorphism alleles, along with determining the karyotype of selected patients. Results: Among similar to 2,500 women with SLE, we found 3 patients with a triple mosaic, consisting of 45,X/46,XX/47,XXX. Among similar to 2,100 women with SS, 1 patient had 45,X/46,XX/47,XXX, with a triplication of the distal p arm of the X chromosome in the 47,XXX cells. Neither the triple mosaic nor the partial triplication was found among the controls. In another SS cohort, we found a mother/daughter pair with partial triplication of this same region of the X chromosome. The triple mosaic occurs in similar to 1 in 25,000-50,000 live female births, while partial triplications are even rarer. Conclusion: Very rare X chromosome abnormalities are present among patients with either SS or SLE and may inform the location of a gene(s) that mediates an X dose effect, as well as critical cell types in which such an effect is operative.

Published
2017
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173. Long-term follow-up in primary Sjögren's syndrome reveals differences in clinical presentation between female and male patients

Author

Sepulveda, Jorge I. Ramirez, Kvarnstrom, Marika, Eriksson, Per, Mandl, Thomas, Norheim, Katrine Braekke, Johnsen, Svein Joar, Hammenfors, Daniel, Jonsson, Malin V., Skarstein, Kathrine, Brun, Johan G., Rönnblom, Lars, Forsblad-d'Elia, Helena, Bucher, Sara Magnusson, Baecklund, Eva, Theander, Elke, Omdal, Roald, Jonsson, Roland, Nordmark, Gunnel, Wahren-Herlenius, Marie, Sepulveda, Jorge I. Ramirez, Kvarnstrom, Marika, Eriksson, Per, Mandl, Thomas, Norheim, Katrine Braekke, Johnsen, Svein Joar, Hammenfors, Daniel, Jonsson, Malin V., Skarstein, Kathrine, Brun, Johan G., Rönnblom, Lars, Forsblad-d'Elia, Helena, Bucher, Sara Magnusson, Baecklund, Eva, Theander, Elke, Omdal, Roald, Jonsson, Roland, Nordmark, Gunnel, and Wahren-Herlenius, Marie

Abstract

Background: Despite men being less prone to develop autoimmune diseases, male sex has been associated with a more severe disease course in several systemic autoimmune diseases. In the present study, we aimed to investigate differences in the clinical presentation of primary Sjogren's syndrome (pSS) between the sexes and establish whether male sex is associated with a more severe form of long-term pSS. Methods: Our study population included 967 patients with pSS (899 females and 68 males) from Scandinavian clinical centers. The mean follow-up time (years) was 8.8 +/- 7.6 for women and 8.5 +/- 6.2 for men (ns). Clinical data including serological and hematological parameters and glandular and extraglandular manifestations were compared between men and women. Results: Male patient serology was characterized by more frequent positivity for anti-Ro/SSA and anti-La/SSB (p = 0. 02), and ANA (p = 0.02). Further, men with pSS were more frequently diagnosed with interstitial lung disease (p = 0. 008), lymphadenopathy (p = 0.04) and lymphoma (p = 0.007). Conversely, concomitant hypothyroidism was more common among female patients (p = 0.009). Conclusions: We observe enhanced serological responses and higher frequencies of lymphoma-related extraglandular manifestations in men with pSS. Notably, lymphoma itself was also significantly more common in men. These observations may reflect an aggravated immune activation and a more severe pathophysiological state in male patients with pSS and indicate a personalized managing of the disease due to the influence of the sex of patients with pSS., Jennifer Meadows is a member of the DISSECT consortium.

Published
2017
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174. H1N1 vaccination in Sjogren's syndrome triggers polyclonal B cell activation and promotes autoantibody production

Author

Brauner, Susanna, Folkersen, Lasse, Kvarnstrom, Marika, Meisgen, Sabrina, Petersen, Sven, Franzen-Malmros, Michaela, Mofors, Johannes, Brokstad, Karl A., Klareskog, Lars, Jonsson, Roland, Westerberg, Lisa S., Trollmo, Christina, Malmstrom, Vivianne, Ambrosi, Aurelie, Kuchroo, Vijay K., Nordmark, Gunnel, Wahren-Herlenius, Marie, Brauner, Susanna, Folkersen, Lasse, Kvarnstrom, Marika, Meisgen, Sabrina, Petersen, Sven, Franzen-Malmros, Michaela, Mofors, Johannes, Brokstad, Karl A., Klareskog, Lars, Jonsson, Roland, Westerberg, Lisa S., Trollmo, Christina, Malmstrom, Vivianne, Ambrosi, Aurelie, Kuchroo, Vijay K., Nordmark, Gunnel, and Wahren-Herlenius, Marie

Abstract

Objectives Vaccination of patients with rheumatic disease has been reported to result in lower antibody titres than in healthy individuals. However, studies primarily include patients on immunosuppressive therapy. Here, we investigated the immune response of treatment-naive patients diagnosed with primary Sjogren's syndrome (pSS) to an H1N1 influenza vaccine. Methods Patients with Sjogren's syndrome without immunomodulatory treatment and age-matched and gender-matched healthy controls were immunised with an H1N1 influenza vaccine and monitored for serological and cellular immune responses. Clinical symptoms were monitored with a standardised form. IgG class switch and plasma cell differentiation were induced in vitro in purified naive B cells of untreated and hydroxychloroquine-treated patients and healthy controls. Gene expression was assessed by NanoString technology. Results Surprisingly, treatment-naive patients with Sjogren's syndrome developed higher H1N1 IgG titres of greater avidity than healthy controls on vaccination. Notably, off-target B cells were also triggered resulting in increased anti-EBV and autoantibody titres. Endosomal toll-like receptor activation of naive B cells in vitro revealed a greater propensity of patient-derived cells to differentiate into plasmablasts and higher production of class switched IgG. The amplified plasma cell differentiation and class switch could be induced in cells from healthy donors by preincubation with type 1 interferon, but was abolished in hydroxychloroquine-treated patients and after in vitro exposure of naive B cells to chloroquine. Conclusions This comprehensive analysis of the immune response in autoimmune patients to exogenous stimulation identifies a mechanistic basis for the B cell hyperactivity in Sjogren's syndrome, and suggests that caution is warranted when considering vaccination in non-treated autoimmune patients.

Published
2017
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175. Identification of a Sjögrens syndrome susceptibility locus at OAS1 that influences isoform switching, protein expression, and responsiveness to type I interferons

Author

Li, He, Ragna Reksten, Tove, Ice, John A., Kelly, Jennifer A., Adrianto, Indra, Rasmussen, Astrid, Wang, Shaofeng, He, Bo, Grundahl, Kiely M., Glenn, Stuart B., Miceli-Richard, Corinne, Bowman, Simon, Lester, Sue, Eriksson, Per, Eloranta, Maija-Leena, Brun, Johan G., Goransson, Lasse G., Harboe, Erna, Guthridge, Joel M., Kaufman, Kenneth M., Kvarnstrom, Marika, Cunninghame Graham, Deborah S., Patel, Ketan, Adler, Adam J., Darise Farris, A., Brennan, Michael T., Chodosh, James, Gopalakrishnan, Rajaram, Weisman, Michael H., Venuturupalli, Swamy, Wallace, Daniel J., Hefner, Kimberly S., Houston, Glen D., Huang, Andrew J. W., Hughes, Pamela J., Lewis, David M., Radfar, Lida, Vista, Evan S., Edgar, Contessa E., Rohrer, Michael D., Stone, Donald U., Vyse, Timothy J., Harley, John B., Gaffney, Patrick M., James, Judith A., Turner, Sean, Alevizos, Ilias, Anaya, Juan-Manuel, Rhodus, Nelson L., Segal, Barbara M., Montgomery, Courtney G., Hal Scofield, R., Kovats, Susan, Mariette, Xavier, Ronnblom, Lars, Witte, Torsten, Rischmueller, Maureen, Wahren-Herlenius, Marie, Omdal, Roald, Jonsson, Roland, Ng, Wan-Fai, Nordmark, Gunnel, Lessard, Christopher J., Sivils, Kathy L., Li, He, Ragna Reksten, Tove, Ice, John A., Kelly, Jennifer A., Adrianto, Indra, Rasmussen, Astrid, Wang, Shaofeng, He, Bo, Grundahl, Kiely M., Glenn, Stuart B., Miceli-Richard, Corinne, Bowman, Simon, Lester, Sue, Eriksson, Per, Eloranta, Maija-Leena, Brun, Johan G., Goransson, Lasse G., Harboe, Erna, Guthridge, Joel M., Kaufman, Kenneth M., Kvarnstrom, Marika, Cunninghame Graham, Deborah S., Patel, Ketan, Adler, Adam J., Darise Farris, A., Brennan, Michael T., Chodosh, James, Gopalakrishnan, Rajaram, Weisman, Michael H., Venuturupalli, Swamy, Wallace, Daniel J., Hefner, Kimberly S., Houston, Glen D., Huang, Andrew J. W., Hughes, Pamela J., Lewis, David M., Radfar, Lida, Vista, Evan S., Edgar, Contessa E., Rohrer, Michael D., Stone, Donald U., Vyse, Timothy J., Harley, John B., Gaffney, Patrick M., James, Judith A., Turner, Sean, Alevizos, Ilias, Anaya, Juan-Manuel, Rhodus, Nelson L., Segal, Barbara M., Montgomery, Courtney G., Hal Scofield, R., Kovats, Susan, Mariette, Xavier, Ronnblom, Lars, Witte, Torsten, Rischmueller, Maureen, Wahren-Herlenius, Marie, Omdal, Roald, Jonsson, Roland, Ng, Wan-Fai, Nordmark, Gunnel, Lessard, Christopher J., and Sivils, Kathy L.

Abstract

Sjogrens syndrome (SS) is a common, autoimmune exocrinopathy distinguished by keratoconjunctivitis sicca and xerostomia. Patients frequently develop serious complications including lymphoma, pulmonary dysfunction, neuropathy, vasculitis, and debilitating fatigue. Dysregulation of type I interferon (IFN) pathway is a prominent feature of SS and is correlated with increased autoantibody titers and disease severity. To identify genetic determinants of IFN pathway dysregulation in SS, we performed cis-expression quantitative trait locus (eQTL) analyses focusing on differentially expressed type I IFN-inducible transcripts identified through a transcriptome profiling study. Multiple cis-eQTLs were associated with transcript levels of 2-5-oligoadenylate synthetase 1 (OAS1) peaking at rs10774671 (PeQTL = 6.05 x 10(-14)). Association of rs10774671 with SS susceptibility was identified and confirmed through meta-analysis of two independent cohorts (P-meta = 2.59 x 10(-9); odds ratio = 0.75; 95% confidence interval = 0.66-0.86). The risk allele of rs10774671 shifts splicing of OAS1 from production of the p46 isoform to multiple alternative transcripts, including p42, p48, and p44. We found that the isoforms were differentially expressed within each genotype in controls and patients with and without autoantibodies. Furthermore, our results showed that the three alternatively spliced isoforms lacked translational response to type I IFN stimulation. The p48 and p44 isoforms also had impaired protein expression governed by the 3 end of the transcripts. The SS risk allele of rs10774671 has been shown by others to be associated with reduced OAS1 enzymatic activity and ability to clear viral infections, as well as reduced responsiveness to IFN treatment. Our results establish OAS1 as a risk locus for SS and support a potential role for defective viral clearance due to altered IFN response as a genetic pathophysiological basis of this complex autoimmune disease., Funding Agencies|NIH [P50AR0608040, 1R01AR065953, 5R01DE015223, 5RC2AR058959, 5P01AR049084, 5P30AR053483, 5U19AI082714, U19AI056363, 1R01DE018209, 5R01DE018209, 8P20GM103456, 1P30GM110766, 1R03AR065786, 5R37AI024717, 5P01AI083194, 7S10RR027190-02, 1U01AI101934, U54GM104938, S10RR026735, 5P30GM103510]; National Institute of Dental and Craniofacial Research; US Department of Veterans Affairs IM MA 9; USA Department of Defense [PR094002]; American College of Rheumatology Research and Education Foundation/Abbott Health Professional Graduate Student Preceptorship Award; Oklahoma Medical Research Foundation; Sjogrens Syndrome Foundation; Phileona Foundation; French ministry of health: PHRC [2006-AOM06133]; French ministry of research [ANR-2010-BLAN-1133]

Published
2017
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176. Distribution of salivary aquaporin-5 in Sjogren's syndrome

Author

Fischer, Axel, Peiser, Christian, Groneberg, David A, Jonsson, Roland, Gordon, Tom P, Hiscock, Jenny, Beroukas, Dimitra, Waterman, Sally A, Delporte, Christine, and Steinfeld, Serge D

Subjects
Sjogren's syndrome -- Physiological aspects, Salivary glands -- Physiological aspects, Lacrimal organs -- Physiological aspects
Published
2002

178. The IRF5-TNPO3 association with systemic lupus erythematosus has two components that other autoimmune disorders variably share

Author

Kottyan, Leah C, Zoller, Erin E, Bene, Jessica, Lu, Xiaoming, Kelly, Jennifer A, Rupert, Andrew M, Lessard, Christopher J, Vaughn, Samuel E, Marion, Miranda, Weirauch, Matthew T, Namjou, Bahram, Adler, Adam, Rasmussen, Astrid, Glenn, Stuart, Montgomery, Courtney G, Hirschfield, Gideon M, Xie, Gang, Coltescu, Catalina, Amos, Chris, Li, He, Ice, John A, Nath, Swapan K, Mariette, Xavier, Bowman, Simon, UK Primary Sjögren's Syndrome Registry, Rischmueller, Maureen, Lester, Sue, Brun, Johan G, Gøransson, Lasse G, Harboe, Erna, Omdal, Roald, Cunninghame-Graham, Deborah S, Vyse, Tim, Miceli-Richard, Corinne, Brennan, Michael T, Lessard, James A, Wahren-Herlenius, Marie, Kvarnström, Marika, Illei, Gabor G, Witte, Torsten, Jonsson, Roland, Eriksson, Per, Nordmark, Gunnel, Ng, Wan-Fai, Anaya, Juan-Manuel, Rhodus, Nelson L, Segal, Barbara M, Merrill, Joan T, James, Judith A, Guthridge, Joel M, Scofield, R Hal, Alarcon-Riquelme, Marta, Bae, Sang-Cheol, Boackle, Susan A, Criswell, Lindsey A, Gilkeson, Gary, Kamen, Diane L, Jacob, Chaim O, Kimberly, Robert, Brown, Elizabeth, Edberg, Jeffrey, Alarcón, Graciela S, Reveille, John D, Vilá, Luis M, Petri, Michelle, Ramsey-Goldman, Rosalind, Freedman, Barry I, Niewold, Timothy, Stevens, Anne M, Tsao, Betty P, Ying, Jun, Mayes, Maureen D, Gorlova, Olga Y, Wakeland, Ward, Radstake, Timothy, Martin, Ezequiel, Martin, Javier, Siminovitch, Katherine, Moser Sivils, Kathy L, Gaffney, Patrick M, Langefeld, Carl D, Harley, John B, and Kaufman, Kenneth M

Subjects
Male, Lupus, Autoimmune Disease, Medical and Health Sciences, Autoimmune Diseases, Cohort Studies, Promoter Regions, Genetic, UK Primary Sjögren's Syndrome Registry, Genetics, Humans, 2.1 Biological and endogenous factors, Polymorphism, Aetiology, Genetics & Heredity, Lupus Erythematosus, Inflammatory and immune system, Systemic, Bayes Theorem, Single Nucleotide, Biological Sciences, beta Karyopherins, DNA-Binding Proteins, Haplotypes, Case-Control Studies, Interferon Regulatory Factors, Biotechnology
Abstract

Exploiting genotyping, DNA sequencing, imputation and trans-ancestral mapping, we used Bayesian and frequentist approaches to model the IRF5-TNPO3 locus association, now implicated in two immunotherapies and seven autoimmune diseases. Specifically, in systemic lupus erythematosus (SLE), we resolved separate associations in the IRF5 promoter (all ancestries) and with an extended European haplotype. We captured 3230 IRF5-TNPO3 high-quality, common variants across 5 ethnicities in 8395 SLE cases and 7367 controls. The genetic effect from the IRF5 promoter can be explained by any one of four variants in 5.7 kb (P-valuemeta = 6 × 10(-49); OR = 1.38-1.97). The second genetic effect spanned an 85.5-kb, 24-variant haplotype that included the genes IRF5 and TNPO3 (P-valuesEU = 10(-27)-10(-32), OR = 1.7-1.81). Many variants at the IRF5 locus with previously assigned biological function are not members of either final credible set of potential causal variants identified herein. In addition to the known biologically functional variants, we demonstrated that the risk allele of rs4728142, a variant in the promoter among the lowest frequentist probability and highest Bayesian posterior probability, was correlated with IRF5 expression and differentially binds the transcription factor ZBTB3. Our analytical strategy provides a novel framework for future studies aimed at dissecting etiological genetic effects. Finally, both SLE elements of the statistical model appear to operate in Sjögren's syndrome and systemic sclerosis whereas only the IRF5-TNPO3 gene-spanning haplotype is associated with primary biliary cirrhosis, demonstrating the nuance of similarity and difference in autoimmune disease risk mechanisms at IRF5-TNPO3.

Published
2015

179. Genetic aspects of Sjögren's syndrome

Author

Bolstad, Anne Isine and Jonsson, Roland

Subjects
Genetic Markers, Male, apoptosis, autoimmune disease, Review, Physical Chromosome Mapping, cytokines, HLA, Disease Models, Animal, Mice, Sjogren's Syndrome, HLA Antigens, Animals, Humans, Female, Genetic Predisposition to Disease, candidate genes, Molecular Biology
Abstract

Sjögren's syndrome is a multisystem inflammatory rheumatic disease that is classified into primary and secondary forms, with cardinal features in the eye (keratoconjunctivitis sicca) and mouth (xerostomia). The aetiology behind this autoimmune exocrinopathy is probably multifactorial and influenced by genetic as well as by environmental factors that are as yet unknown. A genetic predisposition to Sjögren's syndrome has been suggested on the basis of familial aggregation, animal models and candidate gene association studies. Recent advances in molecular and genetic methodologies should further our understanding of this complex disease. The present review synthesizes the current state of genetics in Sjögren's syndrome.

Published
2002

180. The neutrophil protein S100A12 is associated with a comprehensive ultrasonographic synovitis score in a longitudinal study of patients with rheumatoid arthritis treated with adalimumab

Author

Nordal, Hilde Haugedal, Brun, Johan Gorgas, Halse, Anne-Kristine, Jonsson, Roland, Fagerhol, Magne Kristoffer, and Hammer, Hilde Berner

Subjects
Inflammation, Medisinske fag: 700::Klinisk medisinske fag: 750::Reumatologi: 759 [VDP], S100A12, Medisinske Fag: 700 [VDP], Midical sciences: 700::Clinical medical sciences: 750::Rheumatology: 759 [VDP], Orthopedics and Sports Medicine, Rheumatoid arthritis, S100 proteins, Ultrasonography, Biologic therapy
Abstract

Background: The calcium-binding protein S100A12 correlates with measures of disease activity in patients with rheumatoid arthritis (RA). The protein reflects neutrophil activation and the present objective was to explore in a pilot study the associations between S100A12 and other inflammatory markers, clinical assessments as well as degree of synovitis detected by a comprehensive ultrasonography (US) examination in RA patients during biologic treatment. Methods: Twenty patients with RA were examined clinically and by use of US as well as laboratory markers S100A12, calprotectin, C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) before starting adalimumab, with follow-up after 1, 3, 6 and 12 months. Ultrasonographic B-mode (BM) and power Doppler (PD) assessments of 78 joints, 36 tendons/tendon groups and 2 bursas were performed, and sum US scores calculated. Wilcoxon signed rank test assessed treatment response and Spearman rank correlation test was used to calculate correlations. Results: The concentrations of S100A12 decreased after 3 months (p < 0.01) and significant correlations were found between S100A12 and the other laboratory markers during follow-up (0.50-0.62, p < 0.05). Of the clinical assessments, S100A12 had highest correlations with the assessor’s global VAS (0.46-0.85, p < 0.05). Compared with CRP and ESR, S100A12 showed higher correlations with the sum US scores (both BM and PD), with median (range) correlation coefficients of 0.55 (0.35-0.78 (NS-p < 0.001)) for sum BM scores and 0.45 (0.27-0.75 (NS-p < 0.001)) for sum PD scores. Conclusions: The S100A12 protein was significantly associated with other inflammatory markers, clinical assessments as well as sum US scores, indicating that S100A12 is a potential marker of inflammation in RA patients. publishedVersion

Published
2014

181. Altered phenotype and Stat1 expression in Toll-like receptor 7/8 stimulated monocyte-derived dendritic cells from patients with primary Sjögren's syndrome

Author

Vogelsang, Petra, Karlsen, Marie, Brun, Johan G, Jonsson, Roland, and Appel, Silke

Subjects
Rheumatology, Immunology, Immunology and Allergy
Abstract

Introduction: Dendritic cells (DC) are the most potent antigen-presenting cells of the immune system, involved in both initiating immune responses and maintaining tolerance. Dysfunctional and via toll-like receptor (TLR) ligands activated DC have been implicated in the development of autoimmune diseases, but their role in the etiology of Sjögren’s syndrome, a chronic inflammatory autoimmune disease characterized by progressive mononuclear cell infiltration in the exocrine glands, has not been revealed yet. Therefore, the aim of this study was to investigate phenotype and functional properties of immature and TLR7/8 stimulated monocyte-derived DC (moDC) of patients with primary Sjögren’s syndrome (pSS) and compare them to healthy controls. Methods: The phenotype, apoptosis susceptibility and endocytic capacity of moDC were analyzed by flow cytometry. Secretion of cytokines was measured by enzyme-linked immunosorbent assay (ELISA) and multiplex Luminex analyses in moDC cell culture supernatants. The expression of TLR7 was analyzed by flow cytometry and real-time quantitative polymerase chain reaction (qPCR). Expression of Ro/Sjögren’s syndrome-associated autoantigen A (Ro52/SSA), interferon regulatory factor 8 (IRF-8), Bim, signal transduction and activators of transcription (Stat) 1, p-Stat1 (Tyrosin 701), p-Stat1 (Serin 727), Stat3, pStat3 (Tyrosin 705) and glyceraldehyde 3-phosphatase dehydrogenase (GAPDH) was measured by Western blotting. Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) family members were quantified using the ELISA-based TransAM NF-κB family kit. Results: We could not detect differences in expression of co-stimulatory molecules and maturation markers such as cluster of differentiation (CD) 86, CD80, CD40 or CD83 on moDC from patients compared to healthy controls. Moreover, we could not observe variations in apoptosis susceptibility, Bim and Ro52/SSA expression and the endocytic capacity of the moDC. However, we found that moDC from pSS patients expressed increased levels of the major histocompatibility complex (MHC) class II molecule human leukocyte antigen (HLA)-DR. We also found significant differences in cytokine production by moDC, where increased interleukin (IL)-12p40 secretion in mature pSS moDC correlated with increased RelB expression. Strikingly, moDC from pSS patients matured for 48 hours with TLR7/8 ligand CL097 expressed significantly less Stat1. publishedVersion

Published
2014

182. X Chromosome Dose and Sex Bias in Autoimmune Diseases : Increased 47,XXX in Systemic Lupus Erythematosus and Sjögren's Syndrome

Author

Liu, Ke, Kurien, Biji T, Zimmerman, Sarah L, Kaufman, Kenneth M, Taft, Diana H, Kottyan, Leah C, Lazaro, Sara, Weaver, Carrie A, Ice, John A, Adler, Adam J, Chodosh, James, Radfar, Lida, Rasmussen, Astrid, Stone, Donald U, Lewis, David M, Li, Shibo, Koelsch, Kristi A, Igoe, Ann, Talsania, Mitali, Kumar, Jay, Maier-Moore, Jacen S, Harris, Valerie M, Gopalakrishnan, Rajaram, Jonsson, Roland, Lessard, James A, Lu, Xianglan, Gottenberg, Jacques-Eric, Anaya, Juan-Manuel, Cunninghame-Graham, Deborah S, Huang, Andrew J W, Brennan, Michael T, Hughes, Pamela, Illei, Gabor G, Miceli-Richard, Corinne, Keystone, Edward C, Bykerk, Vivian P, Hirschfield, Gideon, Xie, Gang, Ng, Wan-Fai, Nordmark, Gunnel, Eriksson, Per, Omdal, Roald, Rhodus, Nelson L, Rischmueller, Maureen, Rohrer, Michael, Segal, Barbara M, Vyse, Timothy J, Wahren-Herlenius, Marie, Witte, Torsten, Pons-Estel, Bernardo, Alarcon-Riquelme, Marta E, Guthridge, Joel M, James, Judith A, Lessard, Christopher J, Kelly, Jennifer A, Thompson, Susan D, Gaffney, Patrick M, Montgomery, Courtney G, Edberg, Jeffrey C, Kimberly, Robert P, Alarcón, Graciela S, Langefeld, Carl L, Gilkeson, Gary S, Kamen, Diane L, Tsao, Betty P, McCune, W Joseph, Salmon, Jane E, Merrill, Joan T, Weisman, Michael H, Wallace, Daniel J, Utset, Tammy O, Bottinger, Erwin P, Amos, Christopher I, Siminovitch, Katherine A, Mariette, Xavier, Sivils, Kathy L, Harley, John B, Scofield, R Hal, Liu, Ke, Kurien, Biji T, Zimmerman, Sarah L, Kaufman, Kenneth M, Taft, Diana H, Kottyan, Leah C, Lazaro, Sara, Weaver, Carrie A, Ice, John A, Adler, Adam J, Chodosh, James, Radfar, Lida, Rasmussen, Astrid, Stone, Donald U, Lewis, David M, Li, Shibo, Koelsch, Kristi A, Igoe, Ann, Talsania, Mitali, Kumar, Jay, Maier-Moore, Jacen S, Harris, Valerie M, Gopalakrishnan, Rajaram, Jonsson, Roland, Lessard, James A, Lu, Xianglan, Gottenberg, Jacques-Eric, Anaya, Juan-Manuel, Cunninghame-Graham, Deborah S, Huang, Andrew J W, Brennan, Michael T, Hughes, Pamela, Illei, Gabor G, Miceli-Richard, Corinne, Keystone, Edward C, Bykerk, Vivian P, Hirschfield, Gideon, Xie, Gang, Ng, Wan-Fai, Nordmark, Gunnel, Eriksson, Per, Omdal, Roald, Rhodus, Nelson L, Rischmueller, Maureen, Rohrer, Michael, Segal, Barbara M, Vyse, Timothy J, Wahren-Herlenius, Marie, Witte, Torsten, Pons-Estel, Bernardo, Alarcon-Riquelme, Marta E, Guthridge, Joel M, James, Judith A, Lessard, Christopher J, Kelly, Jennifer A, Thompson, Susan D, Gaffney, Patrick M, Montgomery, Courtney G, Edberg, Jeffrey C, Kimberly, Robert P, Alarcón, Graciela S, Langefeld, Carl L, Gilkeson, Gary S, Kamen, Diane L, Tsao, Betty P, McCune, W Joseph, Salmon, Jane E, Merrill, Joan T, Weisman, Michael H, Wallace, Daniel J, Utset, Tammy O, Bottinger, Erwin P, Amos, Christopher I, Siminovitch, Katherine A, Mariette, Xavier, Sivils, Kathy L, Harley, John B, and Scofield, R Hal

Abstract

OBJECTIVE: More than 80% of autoimmune disease is female dominant, but the mechanism for this female bias is poorly understood. We suspected an X chromosome dose effect and hypothesized that trisomy X (47,XXX, 1 in ∼1,000 live female births) would be increased in female predominant diseases (e.g. systemic lupus erythematosus [SLE], primary Sjögren's syndrome [SS], primary biliary cirrhosis [PBC] and rheumatoid arthritis [RA]) compared to diseases without female predominance (sarcoidosis) and controls. METHODS: We identified 47,XXX subjects using aggregate data from single nucleotide polymorphism (SNP) arrays and confirmed, when possible, by fluorescent in situ hybridization (FISH) or quantitative polymerase chain reaction (q-PCR). RESULTS: We found 47,XXX in seven of 2,826 SLE and three of 1,033 SS female patients, but only in two of the 7,074 female controls (p=0.003, OR=8.78, 95% CI: 1.67-86.79 and p=0.02, OR=10.29, 95% CI: 1.18-123.47; respectively). One 47,XXX subject was present for ∼404 SLE women and ∼344 SS women. 47,XXX was present in excess among SLE and SS subjects. CONCLUSION: The estimated prevalence of SLE and SS in women with 47,XXX was respectively ∼2.5 and ∼2.9 times higher than in 46,XX women and ∼25 and ∼41 times higher than in 46,XY men. No statistically significant increase of 47,XXX was observed in other female-biased diseases (PBC or RA), supporting the idea of multiple pathways to sex bias in autoimmunity. This article is protected by copyright. All rights reserved.

Published
2016
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183. Klinefelter's syndrome (47,XXY) is in excess among men with Sjögren's syndrome

Author

Harris, Valerie M., Sharma, Rohan, Cavett, Joshua, Kurien, Biji T, Liu, Ke, Koelsch, Kristi A, Rasmussen, Astrid, Radfar, Lida, Lewis, David, Stone, Donald U, Kaufman, C Erick, Li, Shibo, Segal, Barbara, Wallace, Daniel J, Weisman, Michael H, Venuturupalli, Swamy, Kelly, Jennifer A, Alarcon-Riquelme, Marta E, Pons-Estel, Bernardo, Jonsson, Roland, Lu, Xianglan, Gottenberg, Jacques-Eric, Anaya, Juan-Manuel, Cunninghame-Graham, Deborah S, Huang, Andrew J W, Brennan, Michael T, Hughes, Pamela, Alevizos, Ilias, Miceli-Richard, Corinne, Keystone, Edward C, Bykerk, Vivian P, Hirschfield, Gideon, Xie, Gang, Ng, Wan-Fai, Nordmark, Gunnel, Bucher, Sara Magnusson, Eriksson, Per, Omdal, Roald, Rhodus, Nelson L, Rischmueller, Maureen, Rohrer, Michael, Wahren-Herlenius, Marie, Witte, Torsten, Mariette, Xavier, Lessard, Christopher J, Harley, John B, Sivils, Kathy L, Scofield, R Hal, Harris, Valerie M., Sharma, Rohan, Cavett, Joshua, Kurien, Biji T, Liu, Ke, Koelsch, Kristi A, Rasmussen, Astrid, Radfar, Lida, Lewis, David, Stone, Donald U, Kaufman, C Erick, Li, Shibo, Segal, Barbara, Wallace, Daniel J, Weisman, Michael H, Venuturupalli, Swamy, Kelly, Jennifer A, Alarcon-Riquelme, Marta E, Pons-Estel, Bernardo, Jonsson, Roland, Lu, Xianglan, Gottenberg, Jacques-Eric, Anaya, Juan-Manuel, Cunninghame-Graham, Deborah S, Huang, Andrew J W, Brennan, Michael T, Hughes, Pamela, Alevizos, Ilias, Miceli-Richard, Corinne, Keystone, Edward C, Bykerk, Vivian P, Hirschfield, Gideon, Xie, Gang, Ng, Wan-Fai, Nordmark, Gunnel, Bucher, Sara Magnusson, Eriksson, Per, Omdal, Roald, Rhodus, Nelson L, Rischmueller, Maureen, Rohrer, Michael, Wahren-Herlenius, Marie, Witte, Torsten, Mariette, Xavier, Lessard, Christopher J, Harley, John B, Sivils, Kathy L, and Scofield, R Hal

Abstract

Primary Sjögren's syndrome (pSS) has a strong female bias. We evaluated an X chromosome dose effect by analyzing 47,XXY (Klinefelter's syndrome, 1 in 500 live male births) among subjects with pSS. 47,XXY was determined by examination of fluorescence intensity of single nucleotide polymorphisms from the X and Y chromosomes. Among 136 pSS men there were 4 with 47,XXY. This was significantly different from healthy controls (1 of 1254 had 47,XXY, p=0.0012 by Fisher's exact test) as well men with rheumatoid arthritis (0 of 363 with 47,XXY), but not different compared to men with systemic lupus erythematosus (SLE) (4 of 136 versus 8 of 306, Fisher's exact test p=NS). These results are consistent with the hypothesis that the number of X chromosomes is critical for the female bias of pSS, a property that may be shared with SLE but not RA.

Published
2016
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184. Standardisation of labial salivary gland histopathology in clinical trials in primary Sjögren's syndrome

Author

Fisher, Benjamin A, primary, Jonsson, Roland, additional, Daniels, Troy, additional, Bombardieri, Michele, additional, Brown, Rachel M, additional, Morgan, Peter, additional, Bombardieri, Stefano, additional, Ng, Wan-Fai, additional, Tzioufas, Athanasios G, additional, Vitali, Claudio, additional, Shirlaw, Pepe, additional, Haacke, Erlin, additional, Costa, Sebastian, additional, Bootsma, Hendrika, additional, Devauchelle-Pensec, Valerie, additional, Radstake, Timothy R, additional, Mariette, Xavier, additional, Richards, Andrea, additional, Stack, Rebecca, additional, Bowman, Simon J, additional, and Barone, Francesca, additional

Published
2016
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185. Reply

Author

Jonsson, Roland, primary, Henriksson, Gunnel, additional, and Theander, Elke, additional

Published
2016
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186. Sjögren syndrome

Author

Brito-Zerón, Pilar, primary, Baldini, Chiara, additional, Bootsma, Hendrika, additional, Bowman, Simon J., additional, Jonsson, Roland, additional, Mariette, Xavier, additional, Sivils, Kathy, additional, Theander, Elke, additional, Tzioufas, Athanasios, additional, and Ramos-Casals, Manuel, additional

Published
2016
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187. Klinefelter's syndrome (47,XXY) is in excess among men with Sjögren's syndrome

Author

Harris, Valerie M., primary, Sharma, Rohan, additional, Cavett, Joshua, additional, Kurien, Biji T., additional, Liu, Ke, additional, Koelsch, Kristi A., additional, Rasmussen, Astrid, additional, Radfar, Lida, additional, Lewis, David, additional, Stone, Donald U., additional, Kaufman, C. Erick, additional, Li, Shibo, additional, Segal, Barbara, additional, Wallace, Daniel J., additional, Weisman, Michael H., additional, Venuturupalli, Swamy, additional, Kelly, Jennifer A., additional, Alarcon-Riquelme, Marta E., additional, Pons-Estel, Bernardo, additional, Jonsson, Roland, additional, Lu, Xianglan, additional, Gottenberg, Jacques-Eric, additional, Anaya, Juan-Manuel, additional, Cunninghame-Graham, Deborah S., additional, Huang, Andrew J.W., additional, Brennan, Michael T., additional, Hughes, Pamela, additional, Alevizos, Ilias, additional, Miceli-Richard, Corinne, additional, Keystone, Edward C., additional, Bykerk, Vivian P., additional, Hirschfield, Gideon, additional, Xie, Gang, additional, Ng, Wan-Fai, additional, Nordmark, Gunnel, additional, Bucher, Sara Magnusson, additional, Eriksson, Per, additional, Omdal, Roald, additional, Rhodus, Nelson L., additional, Rischmueller, Maureen, additional, Rohrer, Michael, additional, Wahren-Herlenius, Marie, additional, Witte, Torsten, additional, Mariette, Xavier, additional, Lessard, Christopher J., additional, Harley, John B., additional, Sivils, Kathy L., additional, and Scofield, R. Hal, additional

Published
2016
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190. 3-Day monocyte-derived dendritic cells stimulated with a combination of OK432, TLR7/8 ligand, and prostaglandin E2 are a promising alternative for cancer immunotherapy.

Author

Yi, Dag Heiro, Stetter, Nadine, Jakobsen, Kjerstin, Jonsson, Roland, and Appel, Silke

Subjects
IMMUNOTHERAPY, DENDRITIC cells, CYTOKINES, ANTIGEN presenting cells, CANCER immunotherapy
Abstract

Numerous trials using dendritic cell (DC)-based vaccinations for the treatment of cancer are being carried out. However, an improvement of the quality of DC used is highly warranted. We here generated human monocyte-derived dendritic cells using a 3 day protocol and stimulated the cells using a combination of OK432 (Picibanil), TLR7/8 ligand CL097, and reduced amounts of prostaglandin (PG)E2. We analyzed phenotype, migratory, and T-cell stimulatory capacity compared to a cytokine cocktail consisting of IL-1β, IL-6, TNF, and PGE2. The OK432 cocktail stimulated cells had a similar mature phenotype with upregulated co-stimulatory molecules, HLA-DR and CCR7 as the cytokine cocktail-matured cells and a similar cytokine profile except increased amounts of IL-12p70. Chemotaxis towards CCL19 was reduced compared to the cytokine cocktail, but increased compared to OK432 alone. The T-cell stimulatory capacity was similar to the cytokine cocktail stimulated cells. In conclusion, the OK432 cocktail has the advantage of inducing IL-12p70 production without impairing phenotype or T-cell stimulatory capacity of the cells and might, therefore, be an advantageous alternative to be used in DC-based immunotherapy. [ABSTRACT FROM AUTHOR]

Published
2018
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191. Nobel 2022: An extraordinary achievement relevant to immunity.

Author

Höglund, Petter, Ljunggren, Hans‐Gustaf, and Jonsson, Roland

Subjects
COVID-19, GENETIC transformation, IMMUNITY
Abstract

When immunology was a young discipline, immune cells were studied primarily in the blood of humans and other mammals. This year, Swedish scientist Svante Pääbo, born in Stockholm and with a PhD from Uppsala University, was honoured with the Nobel Prize in Physiology or Medicine. Immunologists, including those from the Radbruch team, will likely identify genes that control the power of the bone marrow in controlling immune memory. [Extracted from the article]

Published
2022
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192. PhD students should be managers, not technicians

Author

Mulvany, Michael J., Jonsson, Roland, and Lackovic, Zdravko

Subjects
PhD study, PhD education
Abstract

Description of current trends in organisation of PhD prigrams in Europe and activities of ORPHEUS.

Published
2012

196. Klinefelter's Syndrome (47,XXY) Among Men with Sjogren's Syndrome

Author

Harris, Valerie M., Cavett, Joshua, Kurien, Biji, Liu, Ke, Koelsch, Kristi A., Radfar, Lida, Lewis, David M., Stone, Donald U., Li, Shibo, Segal, Barbara, Wallace, Daniel J., Weisman, Michael H., Kelly, Jennifer A., Alarcon-Riquelme, Marta, Pons-Estel, Bernado, Jonsson, Roland, Lu, Xianglan, Gottenberg, Jacques, Anaya, Juan-Manuel, Cunninghame-Graham, Deborah S., Keystone, Edward C., Huang, Andrew J. W., Brennan, Michael T., Hughes, Pamela, Illei, G., Miceli, Corinne, Bykerk, V. P., Hirschfield, Gideon, Xie, Gang, Ng, Wan-Fai, Nordmark, Gunnel, Eriksson, Per, Omdal, Roald, Rhodus, Nelson L., Rischmueller, Maureen, Rohrer, Michael D., Wahren-Herlenius, Marie, Witte, Torsten, Mariette, Xavier, Lessard, Christopher, Harley, John B., Sivils, Kathy L., Scofield, Robert Hal, Harris, Valerie M., Cavett, Joshua, Kurien, Biji, Liu, Ke, Koelsch, Kristi A., Radfar, Lida, Lewis, David M., Stone, Donald U., Li, Shibo, Segal, Barbara, Wallace, Daniel J., Weisman, Michael H., Kelly, Jennifer A., Alarcon-Riquelme, Marta, Pons-Estel, Bernado, Jonsson, Roland, Lu, Xianglan, Gottenberg, Jacques, Anaya, Juan-Manuel, Cunninghame-Graham, Deborah S., Keystone, Edward C., Huang, Andrew J. W., Brennan, Michael T., Hughes, Pamela, Illei, G., Miceli, Corinne, Bykerk, V. P., Hirschfield, Gideon, Xie, Gang, Ng, Wan-Fai, Nordmark, Gunnel, Eriksson, Per, Omdal, Roald, Rhodus, Nelson L., Rischmueller, Maureen, Rohrer, Michael D., Wahren-Herlenius, Marie, Witte, Torsten, Mariette, Xavier, Lessard, Christopher, Harley, John B., Sivils, Kathy L., and Scofield, Robert Hal

Published
2015
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197. EULAR Sjögren's syndrome disease activity index (ESSDAI) : a user guide

Author

Seror, Raphaèle, Bowman, Simon J, Brito-Zeron, Pilar, Theander, Elke, Bootsma, Hendrika, Tzioufas, Athanasios, Gottenberg, Jacques-Eric, Ramos-Casals, Manel, Dörner, Thomas, Ravaud, Philippe, Vitali, Claudio, Mariette, Xavier, Asmussen, Karsten, Jacobsen, Soren, Bartoloni, Elena, Gerli, Roberto, Bijlsma, Johannes Wj, Kruize, Aike A, Bombardieri, Stefano, Bookman, Arthur, Kallenberg, Cees, Meiners, Petra, Brun, Johan G, Jonsson, Roland, Caporali, Roberto, Carsons, Steven, De Vita, Salvatore, Del Papa, Nicoletta, Devauchelle, Valerie, Saraux, Alain, Fauchais, Anne-Laure, Sibilia, Jean, Hachulla, Eric, Illei, Gabor, Isenberg, David, Jones, Adrian, Manoussakis, Menelaos, Mandl, Thomas, Jacobsson, Lennart, Demoulins, Frederic, Montecucco, Carlomaurizio, Ng, Wan-Fai, Nishiyama, Sumusu, Omdal, Roald, Parke, Ann, Praprotnik, Sonja, Tomsic, Matjia, Price, Elizabeth, Scofield, Hal, L Sivils, Kathy, Smolen, Josef, Laqué, Roser Solans, Steinfeld, Serge, Sutcliffe, Nurhan, Sumida, Takayuki, Valesini, Guido, Valim, Valeria, Vivino, Frederick B, Vollenweider, Cristina, Seror, Raphaèle, Bowman, Simon J, Brito-Zeron, Pilar, Theander, Elke, Bootsma, Hendrika, Tzioufas, Athanasios, Gottenberg, Jacques-Eric, Ramos-Casals, Manel, Dörner, Thomas, Ravaud, Philippe, Vitali, Claudio, Mariette, Xavier, Asmussen, Karsten, Jacobsen, Soren, Bartoloni, Elena, Gerli, Roberto, Bijlsma, Johannes Wj, Kruize, Aike A, Bombardieri, Stefano, Bookman, Arthur, Kallenberg, Cees, Meiners, Petra, Brun, Johan G, Jonsson, Roland, Caporali, Roberto, Carsons, Steven, De Vita, Salvatore, Del Papa, Nicoletta, Devauchelle, Valerie, Saraux, Alain, Fauchais, Anne-Laure, Sibilia, Jean, Hachulla, Eric, Illei, Gabor, Isenberg, David, Jones, Adrian, Manoussakis, Menelaos, Mandl, Thomas, Jacobsson, Lennart, Demoulins, Frederic, Montecucco, Carlomaurizio, Ng, Wan-Fai, Nishiyama, Sumusu, Omdal, Roald, Parke, Ann, Praprotnik, Sonja, Tomsic, Matjia, Price, Elizabeth, Scofield, Hal, L Sivils, Kathy, Smolen, Josef, Laqué, Roser Solans, Steinfeld, Serge, Sutcliffe, Nurhan, Sumida, Takayuki, Valesini, Guido, Valim, Valeria, Vivino, Frederick B, and Vollenweider, Cristina

Published
2015

198. EULAR Sjögren's syndrome disease activity index (ESSDAI): a user guide

Author

MS Reumatologie/Immunologie/Infectie, Regenerative Medicine and Stem Cells, Infection & Immunity, Seror, Raphaèle, Bowman, Simon J, Brito-Zeron, Pilar, Theander, Elke, Bootsma, Hendrika, Tzioufas, Athanasios, Gottenberg, Jacques-Eric, Ramos-Casals, Manel, Dörner, Thomas, Ravaud, Philippe, Vitali, Claudio, Mariette, Xavier, Asmussen, Karsten, Jacobsen, Soren, Bartoloni, Elena, Gerli, Roberto, Bijlsma, Johannes Wj, Kruize, Aike A, Bombardieri, Stefano, Bookman, Arthur, Kallenberg, Cees, Meiners, Petra, Brun, Johan G, Jonsson, Roland, Caporali, Roberto, Carsons, Steven, De Vita, Salvatore, Del Papa, Nicoletta, Devauchelle, Valerie, Saraux, Alain, Fauchais, Anne-Laure, Sibilia, Jean, Hachulla, Eric, Illei, Gabor, Isenberg, David, Jones, Adrian, Manoussakis, Menelaos, Mandl, Thomas, Jacobsson, Lennart, Demoulins, Frederic, Montecucco, Carlomaurizio, Ng, Wan-Fai, Nishiyama, Sumusu, Omdal, Roald, Parke, Ann, Praprotnik, Sonja, Tomsic, Matjia, Price, Elizabeth, Scofield, Hal, L Sivils, Kathy, Smolen, Josef, Laqué, Roser Solans, Steinfeld, Serge, Sutcliffe, Nurhan, Sumida, Takayuki, Valesini, Guido, Valim, Valeria, Vivino, Frederick B, Vollenweider, Cristina, MS Reumatologie/Immunologie/Infectie, Regenerative Medicine and Stem Cells, Infection & Immunity, Seror, Raphaèle, Bowman, Simon J, Brito-Zeron, Pilar, Theander, Elke, Bootsma, Hendrika, Tzioufas, Athanasios, Gottenberg, Jacques-Eric, Ramos-Casals, Manel, Dörner, Thomas, Ravaud, Philippe, Vitali, Claudio, Mariette, Xavier, Asmussen, Karsten, Jacobsen, Soren, Bartoloni, Elena, Gerli, Roberto, Bijlsma, Johannes Wj, Kruize, Aike A, Bombardieri, Stefano, Bookman, Arthur, Kallenberg, Cees, Meiners, Petra, Brun, Johan G, Jonsson, Roland, Caporali, Roberto, Carsons, Steven, De Vita, Salvatore, Del Papa, Nicoletta, Devauchelle, Valerie, Saraux, Alain, Fauchais, Anne-Laure, Sibilia, Jean, Hachulla, Eric, Illei, Gabor, Isenberg, David, Jones, Adrian, Manoussakis, Menelaos, Mandl, Thomas, Jacobsson, Lennart, Demoulins, Frederic, Montecucco, Carlomaurizio, Ng, Wan-Fai, Nishiyama, Sumusu, Omdal, Roald, Parke, Ann, Praprotnik, Sonja, Tomsic, Matjia, Price, Elizabeth, Scofield, Hal, L Sivils, Kathy, Smolen, Josef, Laqué, Roser Solans, Steinfeld, Serge, Sutcliffe, Nurhan, Sumida, Takayuki, Valesini, Guido, Valim, Valeria, Vivino, Frederick B, and Vollenweider, Cristina

Published
2015

199. EULAR Sjögren's syndrome disease activity index (ESSDAI):a user guide

Author

Seror, Raphaèle, Bowman, Simon J, Brito-Zeron, Pilar, Theander, Elke, Bootsma, Hendrika, Tzioufas, Athanasios, Gottenberg, Jacques-Eric, Ramos-Casals, Manel, Dörner, Thomas, Ravaud, Philippe, Vitali, Claudio, Mariette, Xavier, Asmussen, Karsten, Jacobsen, Soren, Bartoloni, Elena, Gerli, Roberto, Bijlsma, Johannes Wj, Kruize, Aike A, Bombardieri, Stefano, Bookman, Arthur, Kallenberg, Cees, Meiners, Petra, Brun, Johan G, Jonsson, Roland, Caporali, Roberto, Carsons, Steven, De Vita, Salvatore, Del Papa, Nicoletta, Devauchelle, Valerie, Saraux, Alain, Fauchais, Anne-Laure, Sibilia, Jean, Hachulla, Eric, Illei, Gabor, Isenberg, David, Jones, Adrian, Manoussakis, Menelaos, Mandl, Thomas, Jacobsson, Lennart, Demoulins, Frederic, Montecucco, Carlomaurizio, Ng, Wan-Fai, Nishiyama, Sumusu, Omdal, Roald, Parke, Ann, Praprotnik, Sonja, Tomsic, Matjia, Price, Elizabeth, Scofield, Hal, L Sivils, Kathy, Smolen, Josef, Laqué, Roser Solans, Steinfeld, Serge, Sutcliffe, Nurhan, Sumida, Takayuki, Valesini, Guido, Valim, Valeria, Vivino, Frederick B, Vollenweider, Cristina, Seror, Raphaèle, Bowman, Simon J, Brito-Zeron, Pilar, Theander, Elke, Bootsma, Hendrika, Tzioufas, Athanasios, Gottenberg, Jacques-Eric, Ramos-Casals, Manel, Dörner, Thomas, Ravaud, Philippe, Vitali, Claudio, Mariette, Xavier, Asmussen, Karsten, Jacobsen, Soren, Bartoloni, Elena, Gerli, Roberto, Bijlsma, Johannes Wj, Kruize, Aike A, Bombardieri, Stefano, Bookman, Arthur, Kallenberg, Cees, Meiners, Petra, Brun, Johan G, Jonsson, Roland, Caporali, Roberto, Carsons, Steven, De Vita, Salvatore, Del Papa, Nicoletta, Devauchelle, Valerie, Saraux, Alain, Fauchais, Anne-Laure, Sibilia, Jean, Hachulla, Eric, Illei, Gabor, Isenberg, David, Jones, Adrian, Manoussakis, Menelaos, Mandl, Thomas, Jacobsson, Lennart, Demoulins, Frederic, Montecucco, Carlomaurizio, Ng, Wan-Fai, Nishiyama, Sumusu, Omdal, Roald, Parke, Ann, Praprotnik, Sonja, Tomsic, Matjia, Price, Elizabeth, Scofield, Hal, L Sivils, Kathy, Smolen, Josef, Laqué, Roser Solans, Steinfeld, Serge, Sutcliffe, Nurhan, Sumida, Takayuki, Valesini, Guido, Valim, Valeria, Vivino, Frederick B, and Vollenweider, Cristina

Abstract

The EULAR Sjögren's syndrome (SS) disease activity index (ESSDAI) is a systemic disease activity index that was designed to measure disease activity in patients with primary SS. With the growing use of the ESSDAI, some domains appear to be more challenging to rate than others. The ESSDAI is now in use as a gold standard to measure disease activity in clinical studies, and as an outcome measure, even a primary outcome measure, in current randomised clinical trials. Therefore, ensuring an accurate and reproducible rating of each domain, by providing a more detailed definition of each domain, has emerged as an urgent need. The purpose of the present article is to provide a user guide for the ESSDAI. This guide provides definitions and precisions on the rating of each domain. It also includes some minor improvement of the score to integrate advance in knowledge of disease manifestations. This user guide may help clinicians to use the ESSDAI, and increase the reliability of rating and consequently of the ability to detect true changes over time. This better appraisal of ESSDAI items, along with the recent definition of disease activity levels and minimal clinically important change, will improve the assessment of patients with primary SS and facilitate the demonstration of effectiveness of treatment for patients with primary SS.

Published
2015

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