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102. Proceeding Report of the Second Vitiligo International Symposium—November 9–10, 2018, Detroit, Michigan, USA

Author

Lyons, Alexis B., primary, Ghia, Deepti, additional, Abdallah, Marwa, additional, Abdel‐Malek, Zalfa, additional, Esmat, Samia, additional, Ezzedine, Khaled, additional, Grimes, Pearl, additional, Harris, John E., additional, Lui, Harvey, additional, Manga, Prashiela, additional, Mi, Qing‐Sheng, additional, Pandya, Amit, additional, Parsad, Davinder, additional, Passeron, Thiery, additional, Picardo, Mauro, additional, Seneschal, Julien, additional, Silpa‐Archa, Narumol, additional, Taieb, Alain, additional, Xiang, Flora, additional, Lim, Henry W., additional, and Hamzavi, Iltefat H., additional

Published
2020
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108. Validation of a physician global assessment tool for vitiligo extent: Results of an international vitiligo expert meeting

Author

van Geel, Nanja, Wolkerstorfer, Albert, Ezzedine, Khaled, Pandya, Amit G., Bekkenk, Marcel, Grine, Lynda, van Belle, Sarah, Lommerts, Janny E., Hamzavi, Iltefat, Harris, John E., Eleftheriadou, Viktoria, Esmat, Samia, Kang, Hee Young, Kumarasinghe, Prasad, Lan, Cheng-Che E., Parsad, Davinder, Raboobee, Noufal, Flora Xiang, Leihong, Suzuki, Tamio, Prinsen, Cecilia A., Taieb, Alain, Picardo, Mauro, Speeckaert, Reinhart, Anbar, Tag, Anbar, Mohamed, Benzekri, Laïla, Böhm, Markus, Castro, Caïo, Cestari, Tania, Gauthier, Yvon, Gnarra, Maria, Hinojosa, Jorge, Jung, Min Bae, Katayama, Ichiro, Kim, Ki-Ho, Eric Lan, Cheng-Che, Lee, Seung-Chung, le Poole, Caroline, Lim, Henry, Moretti, Silvia, Seneschal, Julien, Spritz, Richard, Xiang, Flora, Dermatology, APH - Methodology, Epidemiology and Data Science, Graduate School, and AII - Inflammatory diseases

Subjects
0301 basic medicine, medicine.medical_specialty, Internationality, Intraclass correlation, Outcome measurements, Vitiligo, Dermatology, Global Health, Risk Assessment, Severity of Illness Index, General Biochemistry, Genetics and Molecular Biology, 03 medical and health sciences, 0302 clinical medicine, medicine, Humans, GeneralLiterature_REFERENCE(e.g.,dictionaries,encyclopedias,glossaries), Reimbursement, ComputingMethodologies_COMPUTERGRAPHICS, Observer Variation, business.industry, Diagnostic Tests, Routine, Outcome measures, Construct validity, Reproducibility of Results, medicine.disease, Inter-rater reliability, 030104 developmental biology, Oncology, 030220 oncology & carcinogenesis, Physical therapy, body surface area, extent, global assessment, outcome measure, severity, vitiligo, Dermatologists, business
Abstract

Currently, vitiligo lacks a validated Physician Global Assessment (PGA) for disease extent. This PGA can be used to stratify and interpret the numeric scores obtained by the Vitiligo Extent Score (VES). We investigated the interrater reliability of a 5-point PGA scale during an international vitiligo workshop. Vitiligo experts from five different continents rated photographs of non-segmental vitiligo patients with varying degrees of extent with the PGA score. Good interrater agreements (intraclass correlation coefficient >0.6) were observed between the raters overall and within each continent. All hypotheses to evaluate construct validity were confirmed. Median VES values per category were for limited 1.10 [IQR: 0.21–1.67], moderate 3.17 [IQR: 1.75–6.21], extensive 9.58 [IQR: 6.21–13.03] and very extensive 42.67 [IQR: 21.20–42.67]. Defined categories for vitiligo extent can be valuable for inclusion criteria and may impact future reimbursement criteria.

Published
2019

109. scRNA-seq of human vitiligo reveals complex networks of subclinical immune activation and a role for CCR5 in Treg function.

Author

Gellatly, Kyle J., Strassner, James P., Essien, Kingsley, Refat, Maggi Ahmed, Murphy, Rachel L., Coffin-Schmitt, Anthony, Pandya, Amit G., Tovar-Garza, Andrea, Frisoli, Michael L., Fan, Xueli, Ding, Xiaolan, Kim, Evangeline E., Abbas, Zainab, McDonel, Patrick, Garber, Manuel, and Harris, John E.

Subjects
T cells, REGULATORY T cells, VITILIGO, LABORATORY mice, RNA sequencing, SKIN diseases
Abstract

Vitiligo allies and villains: Vitiligo is an autoimmune skin disease defined by T cell–mediated destruction of melanocytes. Gellatly et al. (p. 0000) used single-cell RNA sequencing (scRNA-seq) to characterize immune cell subsets that are associated with skin lesions in vitiligo. Type 1 cytokine signaling is a key driver of disease progression, and this signaling pathway was also used by regulatory T cells (Tregs) to limit disease in nonlesional skin. CCR5-CCL5 signaling was critical to effector CD8+ T cell and Treg function, and mouse studies showed that disease suppression required CCR5 expression on Tregs. These studies reveal the complex interactions between immune cell subsets that are involved in vitiligo progression and containment. Vitiligo is an autoimmune skin disease characterized by the targeted destruction of melanocytes by T cells. Cytokine signaling between keratinocytes and T cells results in CD8+ T cell infiltration of vitiligo lesions, but the full scope of signals required to coordinate autoimmune responses is not completely understood. We performed single-cell RNA sequencing on affected and unaffected skin from patients with vitiligo, as well as healthy controls, to define the role of each cell type in coordinating autoimmunity during disease progression. We confirmed that type 1 cytokine signaling occupied a central role in disease, but we also found that this pathway was used by regulatory T cells (Tregs) to restrain disease progression in nonlesional skin. We determined that CCL5-CCR5 signaling served as a chemokine circuit between effector CD8+ T cells and Tregs, and mechanistic studies in a mouse model of vitiligo revealed that CCR5 expression on Tregs was required to suppress disease in vivo but not in vitro. CCR5 was not required for Treg recruitment to skin but appeared to facilitate Treg function by properly positioning these cells within the skin. Our data provide critical insights into the pathogenesis of vitiligo and uncover potential opportunities for therapeutic interventions. [ABSTRACT FROM AUTHOR]

Published
2021
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111. The new musicals

Author

Harris, John E.

Subjects
Musicals -- Criticism and interpretation, Literature/writing, Political science, Sociology and social work
Abstract

The committee for the 1994 series of theater shows in New York theaters had subpar choices for the Best Musical category. New musicals featured included 'Cyrano' and 'Red Shoes.'

Published
1994

112. R & H: kinkier than you think

Author

Harris, John E.

Subjects
Musicals -- Production and direction, Literature/writing, Political science, Sociology and social work
Abstract

Rodgers' and Hammerstein's latest musical productions, 'Allegro' and 'Carousel,' depart from romantic themes for which the two writers are famous for. The vintage musicals feature a Greek chorus to make the music more symphonic.

Published
1994

117. Type I interferon signaling limits viral vector priming of CD8+ T cells during initiation of vitiligo and melanoma immunotherapy.

Author

Riding, Rebecca L., Richmond, Jillian M., Fukuda, Keitaro, and Harris, John E.

Subjects
TYPE I interferons, GENETIC vectors, VITILIGO, MELANOMA, VACCINIA, CYTOTOXIC T cells
Abstract

Vitiligo is an autoimmune skin disease in which epidermal melanocytes are targeted for destruction by CD8+ T cells specific for melanocyte/melanoma‐shared antigens. IFNγ is the central cytokine driving disease, but the role of type I IFN in vitiligo remains unclear. We investigated the functional role of type I IFN during vitiligo progression using two different mouse models: one induced with a vaccinia virus (VV) vaccine and one induced with dendritic cells to prime autoimmune T cells. Induction of vitiligo by VV in IFNaR‐deficient mice led to the development of severe vitiligo compared with wild‐type (WT) mice and was characterized by a significantly enhanced effector CD8+ T‐cell response. Severe vitiligo in this model was a result of VV persistence, because exacerbation of disease in IFNaR‐deficient mice was not observed when antigen‐pulsed dendritic cells were used to induce vitiligo instead of virus. Treatment of B16F10 melanoma‐inoculated mice with VV vaccine therapy also induced a significantly enhanced anti‐tumor response in IFNaR‐deficient mice compared with WT. These results not only help define the pathways responsible for vitiligo progression but also suggest that blockade of type I IFNs following administration of a VV vaccine may provide increased immunogenicity and efficacy for melanoma immunotherapy. [ABSTRACT FROM AUTHOR]

Published
2021
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118. List of Contributors

Author

Abdullah, Anthony, Abel, Mary Kathryn, Abudu, Boya, Abu-Hilal, Mohannad, Al Hammadi, Anwar, Al Awadhi, Ameen, Alexis, Andrew F., Aljefri, Khadija, Al-Kutubi, Huda, Almazan, Timothy H., Almohssen, Amer Ali, Alpsoy, Erkan, Ameen, Mahreen, Anderson, Bryan E., Anshelevich, Ellen, Bacik, Lindsay C., Baker, Donald J., Banach, David, Banfield, Cedric C., Baran, Robert, Barankin, Benjamin, Barkham, Melissa C., Bauer, Johann W., Begun, Zoe, Bell, Michael A., Benton, Emma, Bergfeld, Wilma F., Berman, Brian, Berth-Jones, John, Bhate, Chinmoy, Bhatia, Bhavnit K., Bilgiç, Asli, Bitterman, Avi, Black, Samantha, Blume, Jonathan E., Bohelay, Gérôme, Bordet, Nevianna, Brodell, Robert T., Brown, Marc D., Brownstone, Nicholas D., Burdick, Anne E., Butala, Niraj, Callen, Jeffrey P., Camacho, Ivan D., Camasmie, Helena, Caplivski, Daniel, Cappell, Mitchell S., Casey, Genevieve A., Caux, Frédéric, Chan, Cynthia X., Chan, Lawrence S., Chan, Loi-Yuen, Chan, Stephanie, Chao, Kevin Young, Chen, Jennifer K., Child, Fiona J., Choate, Keith, Chosidow, Olivier, Chousakos, Emmanouil, Chuh, Antonio A.T., Cices, Ahuva, Cobos, Gabriela A., Cohen, Steven R., Collier, Nicholas, Cooper, Elizabeth A., Coulson, Ian H., Cowen, Edward W., Craiglow, Brittany, Cruz, Ponciano D., Jr., Cummins, Donna, Cusack, Carrie Ann R., Daniel, Benjamin S., Daunton, Adam R.A., Davis, Mark D.P., Dawe, Robert S., D’Cruz, David P., de Berker, David, de Brito, Marianne, De Maeseneer, Hannelore, de Moll, Ellen H., Decker, Ashley, DeHoratius, Danielle M., Del Rosso, James Q., Desai, Seemal R., Dhawan, Gaurav K., DiGiovanna, John J., Dodiuk-Gad, Roni P., Duffy, Robert F., Dummer, Reinhard, Dunn, Annie, Duong, Tu-Anh, Dutz, Jan P., Eichenfield, Dawn Z., Eichenfield, Lawrence F., Eisen, Drore, Elman, Scott A., Elston, Dirk M., Elyoussfi, Sarah, Emanuel, Patrick O.M., Enos, Clinton W., Noliza Encarnacion, Maria Rosa, Epstein, Ervin H., Jr., Farberg, Aaron S., Farrugia, Michael E., Fassihi, Hiva, Fawaz, Bilal, Feigenbaum, Lawrence S., Felmingham, Claire, Femia, Alisa, Fenner, Justine, Ferguson, Felicity, Fett, Nicole, Finlay, Andrew Y., Firooz, Alireza, Firoz, Bahar F., Flischel, Amy E., Forrestel, Amy, Foley, Kelly A., Fourzali, Kayla, Frare, Cindy P., Freedman, Derek, Frey, Surina, Fried, Richard, Friedman, Adam J., Fuller, L. Claire, Gabel, Colleen, Gach, Joanna E., Ganesh, Jaya, Ganjoo, Shikhar, Gao, Jing Mia, Gaspari, Anthony A., Glaser, Katherine, Goenaga-Vázquez, Yamila, Goldberg, Leonard H., Goldfarb, Johanna, González Barreto, Reina M., Goon, Peter K.C., Gottlieb, Alice B., Gowda, Asha, Grada, Ayman A., Grande, Donald J., Grant, Matthew, Grattan, Clive E.H., Green, Justin J., Grimes, Pearl E., Gropper, Charles A., Grossberg, Anna L., Gupta, Aditya K., Guttman-Yassky, Emma, Guzman, Anthony K., Haddadi, Nazgol-Sadat, Hadi, Ali S., Hadi, Suhail M., Hagans, Iris A., Hairston, Bethany R., Halpern, Analisa Vincent, Halverstam, Caroline, Haque, Emily, Harries, Matthew, Harris, John E., Haw, William, Hazan, Ezra, Heaton, Henry, Hebert, Adelaide A., Helm, Matthew F., Helms, Stephen E., Hexsel, Camille L., Hexsel, Doris M., Heymann, Warren R., High, Whitney A., Hoffman, Melissa, Horenstein, Marcelo G., Hurst, Eva A., Hussain, Walayat, Ibbotson, Sally H., Ibrahim, Sherrif F., Inamadar, Arun C., Ingen-Housz-Oro, Saskia, Iorizzo, Matilde, Jacobe, Heidi, James, William D., Jemec, Gregor B.E., Jennings, Tara, Jibbe, Atieh S., Johnston, Graham A., Joly, Pascal, Joseph, Adrienne, Kanelleas, Antonios, Karadağ, Ayşe Serap, Katugampola, Ruwani P., Katz, Bruce E., Kavanagh, Gina M., Khan, Sidra S., Khattri, Saakshi, Khong, Brendan, Khorasani, Hooman, Kim, Ellen J., Kim, Hee J., Kim, Youn H., King, Brett, Kirby, Joslyn S., Kirby, Lisa, Kirsner, Robert S., Ko, Lauren, Koch, Dimitra, Koh, Wei-Liang, Koo, John Y.M., Kopp, Sandra A., Kouby, Floriane, Kovarik, Carrie, Kraemer, Kenneth H., Kreeshan, Firas C., Krishnamurthy, Karthik, Kroshinsky, Daniela, Krueger, Steven, Kvernebo, Knut, Laimer, Martin, Lalor, Leah, Lam, Charlene, Lambert, Peter C., Lang, Claudia, Lawlor, Frances, Lawrence, Naomi, Layher, Heather, Lebwohl, Mark G., Lebwohl, Oscar, Lee, Helen, Lehman, Julia S., Lemieux, Alexandre, Leslie, Tabi A., Leung, Alexander K.C., Levitt, Jacob O., Lewis, Daniel J., Lewis, Fiona M., Liaqat, Maryam, Ling, Tsui Chin, Litchman, Graham H., Liu, Stephanie, Luger, Thomas A., Luna, Paula C., Lupi, Omar, Lyon, Calum C., Maatouk, Ismael, MacGibeny, Margaret A., Maddukuri, Spandana, Mahmoud, Bassel H., Makkar, Timothy, Mallett, Richard B., Malta, Kiana, Manci, Rachel, Mancuso, Jennifer, Manders, Steven, Mann, Jasmine, Marghoob, Ashfaq A., Markova, Alina, Markowitz, Orit, Martinez, Daniela, Martinka, Michal, Maurer, Marcus, McGee, Jean S., McLarney, R. Matthew, Meah, Nekma, Metz, Martin, Micali, Giuseppe, Michalik, Daniel, Micheletti, Robert G., Mirowski, Ginat W., Mori, Shoko, Mørk, Cato, Morris, Caroline R., Morton, Colin A., Motaparthi, Kiran, Muldoon, Eavan G., Murase, Jenny E., Murdoch, Michele E., Murrell, Dedee F., Muthiah, Shareen, Myers, Bridget, Naeem, Zunaira, Nakamura, Mio, Nambi, Rabindranath, Nasca, Maria R., Navarrete-Dechent, Cristian, Needham, Glen R., Nehal, Kishwer, Newell, Glenn C., Nixon, Rosemary L., Noy, Mariana L., Nunns, David, Olbricht, Suzanne M., Oldenburg, Reid, Orekoya, Fikki, Osborne, Ruth A., Owen, Cindy E., Pandya, Amit G., Papaefthymiou, Vasileios, Paravar, Taraneh, Parish, Jennifer L., Parish, Lawrence Charles, Perz, Allison M., Peterson, Danielle, Phelps, Robert G., Philips, Rebecca C., Phillips, Tania J., Poh-Fitzpatrick, Maureen B., Polansky, Maxim, Pomeranz, Miriam Keltz, Pope, Elena, Privalle, Ashley N., Prost, Catherine, Que, Syril Keena T., Quint, Koen, Qureshi, Sumera, Rashid, Rabia S., Rashighi, Mehdi, Ratnavel, Ravi, Rawi, Sarah, Reddy, Vidhatha, Renzi, Michael A., Jr., Revuz, Jean, Richard, Gabriele, Rigel, Darrell S., Rivera, Sydney, Robles, Wanda S., Rodriguez, Ramiro, Jr., Rook, Alain H., Rosen, Ted, Rosenbach, Misha, Rowland, Emma, Rustin, Malcolm, Sadlier, Muriel, Salavastru, Carmen Maria, Samimi, Sara, Sandoval, Erika Romero, Sarkany, Robert P.E., Scerri, Lawrence, Schimmel, Joshua, Schmults, Chrysalyne D., Schnur, Rhonda E., Schoinas, Spyridon, Schwartz, Robert A., Scorer, Matthew J., Shah, Kalee, Shah, Nidhi, Shah, Radhika, Shah, Sheevam, Sharif, Jennifer, Shea, Christopher R., Shear, Neil H., Sheriff, Tabrez, Shields, Bridget E., Shimizu, Hiroshi, Shinkai, Kanade, Shiu, Jessica, Shivanna, Ragunatha, Shwayder, Tor, Silverberg, Nanette, Sinclair, Rodney, Singal, Archana, Smith, Janellen, Snyder, Margaret L., Sommer, Lacy L., Soter, Nicholas A., Stanger, Roselyn K., Stoll, Joseph R., Sun, Qisi, Sunderkötter, Cord, Swali, Ritu, Taibjee, Saleem M., Talasila, Sreya, Talebi-Liasi, Faezeh, Tamura, Deborah, Tan, Eunice, Y.-M. Tang, William, Thibodeaux, Quinn, Tian, Tina M., Tiplica, George Sorin, Tkachenko, Elizabeth, Tolkachjov, Stanislav N., Tolliver, Starling D., Tomecki, Kenneth, Torgerson, Rochelle R., Tosti, Antonella, Tsuji-Abe, Yukiko, Twaij, Sara, Tyring, Stephen K., van de Kerkhof, Peter, Van Gysel, Dirk, Van Voorhees, Abby S., Varma, Aakaash, Vasani, Resham, Verma, Shyam B., Vermeer, Maarten H., Vieira, Carlos, Vignes, Stéphane, Vleugels, Ruth Ann, Wallengren, Joanna, Wanat, Karolyn A., Wang, Erica B., Wei, Chapman, Weichert, Gabriele, Weigelt, Maximillian A., Weinberg, Jeffrey M., Weitzer, Danielle, Welponer, Tobias, Werth, Victoria P., White, Lucile E., Wilkin, Jonathan K., Wilson, Niall, Wiznia, Lauren E., Wollenberg, Andreas, Wollina, Uwe, Chun Wong, Junie Li, Wright, Andrew L., Wynne, Matthew, Yan, Daisy, Yosipovitch, Gil, Youssef, Molly J., Zaenglein, Andrea L., Zaki, Irshad, Zarbo, Allison, Zawar, Vijay, Zhu, Jane L., Zone, John J., and Zuberbier, Torsten

Published
2022
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127. Antibody blockade of IL-15 signaling has the potential to durably reverse vitiligo

Author

Richmond, Jillian M., primary, Strassner, James P., additional, Zapata, Lucio, additional, Garg, Madhuri, additional, Riding, Rebecca L., additional, Refat, Maggi A., additional, Fan, Xueli, additional, Azzolino, Vincent, additional, Tovar-Garza, Andrea, additional, Tsurushita, Naoya, additional, Pandya, Amit G., additional, Tso, J. Yun, additional, and Harris, John E., additional

Published
2018
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131. Alopecia areata is a medical disease

Author

Korta, Dorota Z., primary, Christiano, Angela M., additional, Bergfeld, Wilma, additional, Duvic, Madeleine, additional, Ellison, Abby, additional, Fu, Jennifer, additional, Harris, John E., additional, Hordinsky, Maria K., additional, King, Brett, additional, Kranz, Dory, additional, Mackay-Wiggan, Julian, additional, McMichael, Amy, additional, Norris, David A., additional, Price, Vera, additional, Shapiro, Jerry, additional, and Atanaskova Mesinkovska, Natasha, additional

Published
2018
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145. Requirement for CD28 in Effector Treg Differentiation, CCR6 induction, and Skin Homing

Author

Zhang, Ruan, Borges, Christopher M., Fan, Martin Y., Harris, John E., and Turka, Laurence A.

Subjects
CD4-Positive T-Lymphocytes, Receptors, CCR6, Mice, CD28 Antigens, Cell Movement, Receptors, Antigen, T-Cell, alpha-beta, Animals, hemic and immune systems, chemical and pharmacologic phenomena, Cell Differentiation, T-Lymphocytes, Regulatory, Article, Skin
Abstract

The skin, similar to most nonlymphoid tissues, contains substantial numbers of T cells. Among these, memory T cells serve a sentinel role to protect against pathogens, and regulatory T cells (Tregs) terminate immune responses as a check against unrestrained inflammation. Previously, we created conditional knockout mice with Treg-specific deletion of CD28. Although these mice have normal numbers of Tregs, these cells have lower levels of CTLA-4, PD-1, and CCR6, and the animals develop systemic autoimmunity characterized by prominent skin inflammation. In this study, we have performed a detailed analysis of the skin disease in these mice. Our data show that Treg-expressed CD28 is required for optimal maturation of CD44(lo)CD62L(hi) central Tregs into CD44(hi)CD62L(lo) effector Tregs (eTregs), as well as induction of CCR6 among the cells that do become eTregs. Although CD28-deficient Tregs are able to regulate inflammation normally when injected directly into the skin, they fail to home properly to inflamed skin. Collectively, these results suggest a key role for CD28 costimulation in promoting a central Treg to eTreg transition with appropriate upregulation of chemokine receptors such as CCR6 that are required for tissue homing.

Published
2015

148. The Role of Memory CD8+ T Cells in Vitiligo.

Author

Riding, Rebecca L. and Harris, John E.

Subjects
*VITILIGO, *T cells, *SKIN diseases, *DISEASE relapse, *MEMORY, *THERAPEUTICS
Abstract

Vitiligo is an autoimmune skin disease mediated by autoreactive CD8+ T cells that destroy the pigmentproducing cells of the epidermis, melanocytes, leading to areas of depigmentation. Patients with vitiligo require lifelong treatment to regain and maintain their pigment. Clinical observations uncovered the importance of autoimmune memory in vitiligo because cessation of treatment frequently led to relapse of disease at the site of previous lesions. A subset of memory T cells known as CD8+ resident memory T cells (TRM) are long-lived, nonmigratory memory cells that persist in most nonlymphoid tissues, including the skin. Recent reports describe the presence of CD8+ TRM in lesional vitiligo patient skin and suggest their role as active players in disease maintenance. In this review, we will discuss the role of skin CD8+ TRM in maintaining disease in vitiligo and the opportunity to target this population to induce a long-lasting reversal of disease. [ABSTRACT FROM AUTHOR]

Published
2019
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149. Single cell RNA-sequencing reveals molecular signatures that distinguish allergic from irritant contact dermatitis

Author

Frisoli, Michael L., Ko, Wei-Che C., Martinez, Nuria, Afshari, Khashayar, Wang, Yuqing, Garber, Manuel, and Harris, John E.

Abstract

Allergic contact dermatitis (ACD) is a pruritic skin disease caused by environmental chemicals that induce cell-mediated skin inflammation within susceptible individuals. Irritant contact dermatitis (ICD) is caused by direct damage to the skin barrier by environmental insults. Diagnosis can be challenging as both types of contact dermatitis can appear similar by visual exam, and histopathological analysis does not reliably distinguish ACD from ICD. To discover specific biomarkers of ACD and ICD, we characterized the transcriptomic and proteomic changes that occur within the skin during each type of contact dermatitis. We induced ACD and ICD in healthy human volunteers and sampled skin using a non-scarring suction blister biopsy method that collects interstitial fluid and cellular infiltrate. Single cell RNA-sequencing analysis revealed that cell-specific transcriptome differences rather than cell type proportions best distinguished ACD from ICD. Allergy-specific genes were associated with upregulation of IFNG, and cell signaling network analysis implicated several other genes such as IL4,despite their low expression levels. We validated transcriptomic differences with proteomic assays on blister fluid and trained a logistic regression model on skin interstitial fluid proteins that could distinguish ACD from ICD and healthy control skin with 93% sensitivity and 93% specificity.

Published
2024
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150. CXCR4 identifies transitional bone marrow premonocytes that replenish the mature monocyte pool for peripheral responses

Author

Chong, Shu Zhen, primary, Evrard, Maximilien, additional, Devi, Sapna, additional, Chen, Jinmiao, additional, Lim, Jyue Yuan, additional, See, Peter, additional, Zhang, Yiru, additional, Adrover, José M., additional, Lee, Bernett, additional, Tan, Leonard, additional, Li, Jackson L.Y., additional, Liong, Ka Hang, additional, Phua, Cindy, additional, Balachander, Akhila, additional, Boey, Adrian, additional, Liebl, David, additional, Tan, Suet Mien, additional, Chan, Jerry K.Y., additional, Balabanian, Karl, additional, Harris, John E., additional, Bianchini, Mariaelvy, additional, Weber, Christian, additional, Duchene, Johan, additional, Lum, Josephine, additional, Poidinger, Michael, additional, Chen, Qingfeng, additional, Rénia, Laurent, additional, Wang, Cheng-I, additional, Larbi, Anis, additional, Randolph, Gwendalyn J., additional, Weninger, Wolfgang, additional, Looney, Mark R., additional, Krummel, Matthew F., additional, Biswas, Subhra K., additional, Ginhoux, Florent, additional, Hidalgo, Andrés, additional, Bachelerie, Françoise, additional, and Ng, Lai Guan, additional

Published
2016
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