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7. Identification of 15 new psoriasis susceptibility loci highlights the role of innate immunity

Author

Tsoi, Lam C, Spain, Sarah L, Knight, Jo, Ellinghaus, Eva, Stuart, Philip E, Capon, Francesca, Ding, Jun, Li, Yanming, Tejasvi, Trilokraj, Gudjonsson, Johann E, Kang, Hyun M, Allen, Michael H, McManus, Ross, Novelli, Giuseppe, Samuelsson, Lena, Schalkwijk, Joost, Ståhle, Mona, Burden, A David, Smith, Catherine H, Cork, Michael J, Estivill, Xavier, Bowcock, Anne M, Krueger, Gerald G, Weger, Wolfgang, Worthington, Jane, Tazi-Ahnini, Rachid, Nestle, Frank O, Hayday, Adrian, Hoffmann, Per, Winkelmann, Juliane, Wijmenga, Cisca, Langford, Cordelia, Edkins, Sarah, Andrews, Robert, Blackburn, Hannah, Strange, Amy, Band, Gavin, Pearson, Richard D, Vukcevic, Damjan, Spencer, Chris CA, Deloukas, Panos, Mrowietz, Ulrich, Schreiber, Stefan, Weidinger, Stephan, Koks, Sulev, Kingo, Külli, Esko, Tonu, Metspalu, Andres, Lim, Henry W, Voorhees, John J, Weichenthal, Michael, Wichmann, H Erich, Chandran, Vinod, Rosen, Cheryl F, Rahman, Proton, Gladman, Dafna D, Griffiths, Christopher EM, Reis, Andre, Kere, Juha, Nair, Rajan P, Franke, Andre, Barker, Jonathan NWN, Abecasis, Goncalo R, Elder, James T, and Trembath, Richard C

Subjects
Genetics, Autoimmune Disease, Human Genome, Psoriasis, Aetiology, 2.1 Biological and endogenous factors, Skin, CARD Signaling Adaptor Proteins, Core Binding Factor Alpha 3 Subunit, DEAD Box Protein 58, DEAD-box RNA Helicases, GTPase-Activating Proteins, Genetic Loci, Genetic Predisposition to Disease, Genome-Wide Association Study, Guanylate Cyclase, Humans, Immunity, Innate, Membrane Proteins, Oligonucleotide Array Sequence Analysis, Polymorphism, Single Nucleotide, Receptors, Immunologic, STAT3 Transcription Factor, T-Lymphocytes, White People, Collaborative Association Study of Psoriasis, Genetic Analysis of Psoriasis Consortium, Psoriasis Association Genetics Extension, Wellcome Trust Case Control Consortium 2, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

To gain further insight into the genetic architecture of psoriasis, we conducted a meta-analysis of 3 genome-wide association studies (GWAS) and 2 independent data sets genotyped on the Immunochip, including 10,588 cases and 22,806 controls. We identified 15 new susceptibility loci, increasing to 36 the number associated with psoriasis in European individuals. We also identified, using conditional analyses, five independent signals within previously known loci. The newly identified loci shared with other autoimmune diseases include candidate genes with roles in regulating T-cell function (such as RUNX3, TAGAP and STAT3). Notably, they included candidate genes whose products are involved in innate host defense, including interferon-mediated antiviral responses (DDX58), macrophage activation (ZC3H12C) and nuclear factor (NF)-κB signaling (CARD14 and CARM1). These results portend a better understanding of shared and distinctive genetic determinants of immune-mediated inflammatory disorders and emphasize the importance of the skin in innate and acquired host defense.

Published
2012

8. Multiple common variants for celiac disease influencing immune gene expression

Author

Dubois, Patrick CA, Trynka, Gosia, Franke, Lude, Hunt, Karen A, Romanos, Jihane, Curtotti, Alessandra, Zhernakova, Alexandra, Heap, Graham AR, Ádány, Róza, Aromaa, Arpo, Bardella, Maria Teresa, van den Berg, Leonard H, Bockett, Nicholas A, de la Concha, Emilio G, Dema, Bárbara, Fehrmann, Rudolf SN, Fernández-Arquero, Miguel, Fiatal, Szilvia, Grandone, Elvira, Green, Peter M, Groen, Harry JM, Gwilliam, Rhian, Houwen, Roderick HJ, Hunt, Sarah E, Kaukinen, Katri, Kelleher, Dermot, Korponay-Szabo, Ilma, Kurppa, Kalle, MacMathuna, Padraic, Mäki, Markku, Mazzilli, Maria Cristina, McCann, Owen T, Mearin, M Luisa, Mein, Charles A, Mirza, Muddassar M, Mistry, Vanisha, Mora, Barbara, Morley, Katherine I, Mulder, Chris J, Murray, Joseph A, Núñez, Concepción, Oosterom, Elvira, Ophoff, Roel A, Polanco, Isabel, Peltonen, Leena, Platteel, Mathieu, Rybak, Anna, Salomaa, Veikko, Schweizer, Joachim J, Sperandeo, Maria Pia, Tack, Greetje J, Turner, Graham, Veldink, Jan H, Verbeek, Wieke HM, Weersma, Rinse K, Wolters, Victorien M, Urcelay, Elena, Cukrowska, Bozena, Greco, Luigi, Neuhausen, Susan L, McManus, Ross, Barisani, Donatella, Deloukas, Panos, Barrett, Jeffrey C, Saavalainen, Paivi, Wijmenga, Cisca, and van Heel, David A

Subjects
Biotechnology, Human Genome, Genetics, Digestive Diseases, 2.1 Biological and endogenous factors, Aetiology, Case-Control Studies, Celiac Disease, Gene Expression, Gene Expression Profiling, Genes, MHC Class I, Genome-Wide Association Study, Humans, Meta-Analysis as Topic, Polymorphism, Single Nucleotide, Risk, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

We performed a second-generation genome-wide association study of 4,533 individuals with celiac disease (cases) and 10,750 control subjects. We genotyped 113 selected SNPs with P(GWAS) < 10(-4) and 18 SNPs from 14 known loci in a further 4,918 cases and 5,684 controls. Variants from 13 new regions reached genome-wide significance (P(combined) < 5 x 10(-8)); most contain genes with immune functions (BACH2, CCR4, CD80, CIITA-SOCS1-CLEC16A, ICOSLG and ZMIZ1), with ETS1, RUNX3, THEMIS and TNFRSF14 having key roles in thymic T-cell selection. There was evidence to suggest associations for a further 13 regions. In an expression quantitative trait meta-analysis of 1,469 whole blood samples, 20 of 38 (52.6%) tested loci had celiac risk variants correlated (P < 0.0028, FDR 5%) with cis gene expression.

Published
2010

12. Comparative Genetic Analysis of Psoriatic Arthritis and Psoriasis for the Discovery of Genetic Risk Factors and Risk Prediction Modeling

Author

Soomro, Mehreen, Stadler, Michael, Dand, Nick, Bluett, James, Jadon, Deepak, Jalali-Najafabadi, Farideh, Duckworth, Michael, Ho, Pauline, Marzo-Ortega, Helena, Helliwell, Philip S, Ryan, Anthony W, Kane, David, Korendowych, Eleanor, Simpson, Michael A, Packham, Jonathan, McManus, Ross, Gabay, Cem, Lamacchia, Céline, Nissen, Michael J, Brown, Matthew A, Verstappen, Suzanne MM, Van Staa, Tjeerd, Barker, Jonathan N, Smith, Catherine H, BADBIR Study Group, BSTOP Study Group, FitzGerald, Oliver, McHugh, Neil, Warren, Richard B, Bowes, John, Barton, Anne, Stadler, Michael [0000-0003-3689-4256], Helliwell, Philip S [0000-0002-4155-9105], McManus, Ross [0000-0002-0529-9617], Lamacchia, Céline [0000-0002-0291-8865], and Apollo - University of Cambridge Repository

Subjects
Biological Products, Risk Factors, Case-Control Studies, Arthritis, Psoriatic, Humans, Psoriasis, Genetic Predisposition to Disease
Abstract

Funder: Cambridge Arthritis Research Endeavour (CARE), Funder: Leeds NIHR Biomedical Research Centre, Funder: Manchester NIHR Biomedical Research Centre, Funder: National Institute for Health Research; Id: http://dx.doi.org/10.13039/501100000272, Funder: NIHR Manchester BRC; Id: http://dx.doi.org/10.13039/100014653, OBJECTIVES: Psoriatic arthritis (PsA) has a strong genetic component, and the identification of genetic risk factors could help identify the ~30% of psoriasis patients at high risk of developing PsA. Our objectives were to identify genetic risk factors and pathways that differentiate PsA from cutaneous-only psoriasis (PsC) and to evaluate the performance of PsA risk prediction models. METHODS: Genome-wide meta-analyses were conducted separately for 5,065 patients with PsA and 21,286 healthy controls and separately for 4,340 patients with PsA and 6,431 patients with PsC. The heritability of PsA was calculated as a single-nucleotide polymorphism (SNP)-based heritability estimate (h2 SNP ) and biologic pathways that differentiate PsA from PsC were identified using Priority Index software. The generalizability of previously published PsA risk prediction pipelines was explored, and a risk prediction model was developed with external validation. RESULTS: We identified a novel genome-wide significant susceptibility locus for the development of PsA on chromosome 22q11 (rs5754467; P = 1.61 × 10-9 ), and key pathways that differentiate PsA from PsC, including NF-κB signaling (adjusted P = 1.4 × 10-45 ) and Wnt signaling (adjusted P = 9.5 × 10-58 ). The heritability of PsA in this cohort was found to be moderate (h2 SNP = 0.63), which was similar to the heritability of PsC (h2 SNP = 0.61). We observed modest performance of published classification pipelines (maximum area under the curve 0.61), with similar performance of a risk model derived using the current data. CONCLUSION: Key biologic pathways associated with the development of PsA were identified, but the investigation of risk classification revealed modest utility in the available data sets, possibly because many of the PsC patients included in the present study were receiving treatments that are also effective in PsA. Future predictive models of PsA should be tested in PsC patients recruited from primary care.

Published
2022

13. Childhood trauma, IL-6 and weaker suppression of the default mode network (DMN) during theory of mind (ToM) performance in schizophrenia

Author

King, Sinead, primary, Mothersill, David, additional, Holleran, Laurena, additional, Patlola, Saahithh, additional, McManus, Ross, additional, Kenyon, Marcus, additional, McDonald, Colm, additional, Hallahan, Brian, additional, Corvin, Aiden, additional, Morris, Derek W., additional, Kelly, John P., additional, McKernan, Declan, additional, and Donohoe, Gary, additional

Published
2022
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15. Replication of a distinct psoriatic arthritis risk variant at the IL23R locus

Author

Budu-Aggrey, Ashley, Bowes, John, Loehr, Sabine, Uebe, Steffen, Zervou, Maria I, Helliwell, Philip, Ryan, Anthony W, Kane, David, Korendowych, Eleanor, Giardina, Emiliano, Packham, Jonathan, McManus, Ross, FitzGerald, Oliver, McHugh, Neil, Behrens, Frank, Burkhardt, Harald, Huffmeier, Ulrike, Ho, Pauline, Martin, Javier, Castañeda, Santos, Goulielmos, George, Reis, Andre, and Barton, Anne

Published
2016
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16. Cross-phenotype association mapping of the MHC identifies genetic variants that differentiate psoriatic arthritis from psoriasis

Author

Bowes, John, Ashcroft, James, Dand, Nick, Jalali-najafabadi, Farideh, Bellou, Eftychia, Ho, Pauline, Marzo-Ortega, Helena, Helliwell, Philip S, Feletar, Marie, Ryan, Anthony W, Kane, David J, Korendowych, Eleanor, Simpson, Michael A, Packham, Jonathan, McManus, Ross, Brown, Matthew A, Smith, Catherine H, Barker, Jonathan N, McHugh, Neil, FitzGerald, Oliver, Warren, Richard B, and Barton, Anne

Published
2017
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17. Increased Population Risk of AIP‐Related Acromegaly and Gigantism in Ireland

Author

Radian, Serban, Diekmann, Yoan, Gabrovska, Plamena, Holland, Brendan, Bradley, Lisa, Wallace, Helen, Stals, Karen, Bussell, Anna‐Marie, McGurren, Karen, Cuesta, Martin, Ryan, Anthony W., Herincs, Maria, Hernández‐Ramírez, Laura C., Holland, Aidan, Samuels, Jade, Aflorei, Elena Daniela, Barry, Sayka, Dénes, Judit, Pernicova, Ida, Stiles, Craig E., Trivellin, Giampaolo, McCloskey, Ronan, Ajzensztejn, Michal, Abid, Noina, Akker, Scott A., Mercado, Moises, Cohen, Mark, Thakker, Rajesh V., Baldeweg, Stephanie, Barkan, Ariel, Musat, Madalina, Levy, Miles, Orme, Stephen M., Unterländer, Martina, Burger, Joachim, Kumar, Ajith V., Ellard, Sian, McPartlin, Joseph, McManus, Ross, Linden, Gerard J., Atkinson, Brew, Balding, David J., Agha, Amar, Thompson, Chris J., Hunter, Steven J., Thomas, Mark G., Morrison, Patrick J., and Korbonits, Márta

Published
2017
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18. Study protocol for the St James's Hospital, Tallaght University Hospital, Trinity College Dublin Allied Researchers' (STTAR) Bioresource for COVID-19

Author

O'Doherty, Laura, primary, Hendricken Phelan, Stuart, additional, Wood, Nicole, additional, O'Brien, Sorcha, additional, Sui, Jacklyn, additional, Mangan, Cian, additional, Howley, Fergal, additional, O'Regan, Siobhan, additional, Razif, Noor Adeebah Mohamed, additional, Conlan, Ciara, additional, Argue, Ruth, additional, Holohan, Samuel, additional, Dyer, Adam, additional, Salleh, Fara, additional, Townsend, Liam, additional, Hughes, Gerard, additional, Kerr, Colm, additional, Reidy, Derval, additional, Sanz, Alberto, additional, Connolly, Emma, additional, Kelly, Andrea, additional, Leacy, Emma, additional, Reddy, Conor, additional, Gargan, Siobhan, additional, Breen, Eamon, additional, Hawerkamp, Heike, additional, Dunne, Jean, additional, Martin-Loeches, Ignacio, additional, McLaughlin, Anne Marie, additional, Long, Aideen, additional, Shiels, Orla, additional, Fallon, Padraic, additional, Hennessy, Martina, additional, Romero-Ortuno, Roman, additional, Bannan, Ciaran, additional, Prior, Anna Rose, additional, Rakovac, Ana, additional, McCormack, William, additional, McManus, Ross, additional, Donnelly, Seamus, additional, Bergin, Colm, additional, Little, Mark, additional, Ní Cheallaigh, Clíona, additional, and Conlon, Niall, additional

Published
2022
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19. Study Protocol for the St James's Hospital, Tallaght University Hospital, Trinity College Dublin Allied Researchers' (STTAR) Bioresource for COVID-19

Author

O'Doherty, Laura, Hendricken Phelan, Stuart, Wood, Nicole, O'Brien, Sorcha, O'Regan, S, Sui, Jacklyn, Mohammed, Noor Adeebah, Mangan, Cian, Salleh, Fara, Dyer, Adam, Howley, Fergal, Kerr, Colm, Conlan, Ciara, Holohan, Samuel, Hughes, Gerry, Reidy, Derval, Sanz, Alberto, Argue, Ruth, Townsend, Liam, Connolly, Emma, Kelly, Andrea, Leacy, Emma, Reddy, Conor, Gargan, Siobhan, Breen, Eamon, Hawerkamp, Heike, Dunne, Jean, Martin Loeches, Ignatio, McLaughlin, Anne Marie, Long, Aideen, Shiels, Orla, Fallon, Padriac, Hennessy, Martina, Bannan, Ciaran, Prior, Anna Rose, Rakovac, Ana, McManus, Ross, Romero-Ortuno, Roman, McCormack, Willam, Donnelly, Seamus, Bergin, Colm, Little, Mark, Ní Cheallaigh, Clíona, and Conlon, Niall

Subjects
COVID-19, Biobank, Vaccine
Abstract

Appendices for STTAR Bioresource COVID-19 Biobanking study. The primary objective of this study is to build a biobank, to understand the clinical characteristics and natural history of COVID-19 infection with the long-term goal of research into improved disease understanding, diagnostic tests and treatments. These appendices include the case report form, informed consent form and online convalescent visit report form related to this study&nbsp

Published
2022
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27. PTPN22 is associated with susceptibility to psoriatic arthritis but not psoriasis: evidence for a further PsA-specific risk locus

Author

Bowes, John, Loehr, Sabine, Budu-Aggrey, Ashley, Uebe, Steffen, Bruce, Ian N, Feletar, Marie, Marzo-Ortega, Helena, Helliwell, Philip, Ryan, Anthony W, Kane, David, Korendowych, Eleanor, Alenius, Gerd-Marie, Giardina, Emiliano, Packham, Jonathan, McManus, Ross, FitzGerald, Oliver, Brown, Matthew A, Behrens, Frank, Burkhardt, Harald, McHugh, Neil, Huffmeier, Ulrike, Ho, Pauline, Reis, Andre, and Barton, Anne

Published
2015
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29. Leptin receptor polymorphisms interact with polyunsaturated fatty acids to augment risk of insulin resistance and metabolic syndrome in adults

Author

Phillips, Catherine M., Goumidi, Louisa, Bertrais, Sandrine, Field, Martyn R., Ordovas, Jose M., Cupples, L. Adrienne, Defoort, Catherine, Lovegrove, Julie A., Drevon, Christian A., Blaak, Ellen E., Gibney, Michael J., Kiec-Wilk, Beata, Karlstrom, Britta, Lopez-Miranda, Jose, McManus, Ross, Hercberg, Serge, Lairon, Denis, Planells, Richard, and Roche, Helen M.

Subjects
Leptin -- Genetic aspects, Leptin -- Structure, Genetic polymorphisms -- Observations, Food/cooking/nutrition
Abstract

The leptin receptor (LEPR) is associated with insulin resistance, a key feature of metabolic syndrome (MetS). Gene- fatty acid interactions may affect MetS risk. The objective was to investigate the relationship among LEPR polymorphisms, insulin resistance, and MetS risk and whether plasma fatty acids, a biomarker of dietary fatty acids, modulate this. LEPR polymorphisms (rs10493380, rs1137100, rs1137101, rs12067936, rs1805096, rs2025805, rs3790419, rs3790433, rs6673324, and rs8179183), biochemical measurements, and plasma fatty acid profiles were determined in the LIPGENE-SU.VI.MAX study of MetS cases and matched controls (n = 1754). LEPR rs3790433 GG homozygotes had increased MetS risk compared with the minor A allele carriers [odds ratio (OR) = 1.65; 95% CI: 1.05-2.57; P = 0.028], which may be accounted for by their increased risk of elevated insulin concentrations (OR 2.40; 95% CI: 1.28-4.50; P= 0.006) and insulin resistance (OR = 2.15; 95% CI: 1.18-3.90; P= 0.012). Low (less than median) plasma (n-3) and high (n-6) PUFA status exacerbated the genetic risk conferred by GG homozygosity to hyperinsulinemia (OR 2.92-2.94) and insulin resistance (OR 3.40-3.47). Interestingly, these associations were abolished against a high (n-3) or low (n-6) PUFA background. Importantly, we replicated some of these findings in an independent cohort. Homozygosity for the LEPR rs3790433 G allele was associated with insulin resistance, which may predispose to increased MetS risk. Novel gene-nutrient interactions between LEPR rs3790433 and PUFA suggest that these genetic influences were more evident in individuals with low plasma (n-3) or high plasma (n-6) PUFA. J. Nutr. 140: 238-244, 2010. doi: 10.3945/jn.109.115329.

Published
2010

30. Dietary saturated fat modulates the association between STAT3 polymorphisms and abdominal obesity in adults

Author

Phillips, Catherine M., Goumidi, Louisa, Bertrais, Sandrine, Field, Martyn R., Peloso, Gina M., Shen, Jian, McManus, Ross, Hercberg, Serge, Lairon, Denis, Planells, Richard, and Roche, Helen M.

Subjects
Obesity -- Prevention, Dietary fat -- Physiological aspects, Food/cooking/nutrition
Abstract

Signal transducer and activator of transcription 3 (STAT3) plays a key role in body weight regulation and glucose homeostasis, 2 important determinants of metabolic syndrome (MetS). Dietary fat is a key environmental factor that may interact with genotype to affect MetS risk. In this study, we investigated the relationship between STAT3 polymorphisms and MetS phenotypes and determined potential interactions with dietary fatty acids. STAT3 polymorphisms (rs8069645, rs744166, rs2306580, rs2293152, and rs10530050), biochemical measurements, and dietary fat composition were determined in the LIPGENE-SU.VI.MAX study of MetS cases and matched controls (n = 1754). STAT3 polymorphisms were not associated with MetS risk. However, minor G allele carriers for rs8069645, rs744166, and rs1053005 and major GG homozygotes for rs2293152 had increased risk of abdominal obesity compared with noncarriers [odds ratio (OR) = 2.22, P = 0.0005; OR = 2.08, P = 0.0017; OR = 2.00, P = 0.0033; and OR = 1.95, P = 0.028, respectively]. The number of risk alleles additively increased obesity risk (P = 0.0003). Dietary SFA intake exacerbated these effects; among all participants with the highest SFA intake (-> 15.5% of energy), individuals carrying >2 risk alleles had further increased risk of obesity (OR = 3.30; 95% CI = 1.50-7.28; P = 0.0079) compared with those carrying - doi: 10.3945/jn.109.100635

Published
2009

32. Shared and distinct genetic variants in type 1 diabetes and celiac disease

Author

Smyth, Deborah J., Plagnol, Vincent, Walker, Neil M., Cooper, Jason D., Downes, Kate, Yang, Jennie H.M., Howson, Joanna M.M., Stevens, Helen, McManus, Ross, Wijmenga, Cisca, Heap, Graham A., Dubois, Patrick C., Clayton, David G., Hunt, Karen A., van Heel, David A., and Todd, John A.

Subjects
Type 1 diabetes -- Genetic aspects, Type 1 diabetes -- Research, Type 1 diabetes -- Causes of, Celiac disease -- Genetic aspects, Celiac disease -- Research, Celiac disease -- Causes of, Allelomorphism -- Research, Allelomorphism -- Physiological aspects
Abstract

This study investigates whether non-HLA loci are shared by type 1 diabetes and celiac disease, which have a common genetic origin. The results indicate that both type 1 diabetes and celiac disease share common alleles, and might exhibit common biological mechanisms.

Published
2008

33. The human response to infection is associated with distinct patterns of interleukin 23 and interleukin 27 expression

Author

O'Dwyer, Michael J., Mankan, Arun K., White, Mary, Lawless, Mathew W., Stordeur, Patrick, O'Connell, Brian, Kelleher, Dermot P., McManus, Ross, and Ryan, Thomas

Subjects
Interleukins -- Physiological aspects, Interleukins -- Health aspects, Sepsis -- Development and progression, Sepsis -- Genetic aspects, T cells -- Health aspects, T cells -- Genetic aspects, Health care industry
Abstract

Byline: Michael J. O'Dwyer (1,2), Arun K. Mankan (2), Mary White (1), Mathew W. Lawless (2), Patrick Stordeur (3), Brian O'Connell (4), Dermot P. Kelleher (2), Ross McManus (2), Thomas Ryan (1) Keywords: Sepsis syndrome; Cytokines; Reverse transcriptase polymerase chain reaction; Helper T-cells Abstract: Objective The development and progression of severe sepsis is related to a deficiency in pro-inflammatory cytokine production, characterised by lesser IFNI3 levels, which are not explained by variations in levels of the main putative regulator of IFNI3, namely IL-12. As alternative regulators of IFNI3 may be of greater importance in human sepsis, we investigated the hypothesis that the development of severe sepsis is related to variations in IL-18, IL-23 and IL-27 gene expression. Design and setting A prospective observational trial in a mixed intensive care unit (ICU) and hospital wards in a university teaching hospital. Patients and participants Sixty-two ICU patients with severe sepsis, 13 bacteraemic patients with no acute critical illness, and 10 healthy controls. Measurements and results All subjects were assayed for IL-18, IL-23 and IL-27 mRNA levels in peripheral blood. IL-27 mRNA levels distinguished between the three groups, with levels highest in the ICU group, intermediate in the bacteraemic group and lowest in the control group. IL-23 distinguished between the groups, with levels lowest in the ICU group. In late sepsis IL-23 and TNF[alpha] mRNA levels were directly related. IL-18 mRNA levels did not distinguish between the patient groups. Conclusions We conclude that the deficient pro-inflammatory response in patients with sepsis is expansive and includes deficient IL-23 and excessive IL-27 gene expression. This provides further evidence that upregulation of a cytokine-based immune response is beneficial in sepsis. Author Affiliation: (1) Department of Anaesthesia, St James's Hospital, Dublin, Ireland (2) Department of Clinical Medicine, Trinity College, Dublin, Ireland (3) Department of Immunology-Haematology-Transfusion, Hopital Erasme, Universite Libre de Bruxelles, Brussels, Belgium (4) Department of Clinical Microbiology, St James's Hospital, Dublin, Ireland Article History: Registration Date: 27/11/2007 Received Date: 15/08/2007 Accepted Date: 25/11/2007 Online Date: 29/01/2008 Article note: Electronic supplementary material The online version of this article (doi: 10.1007/s00134-007-0968-5) contains supplementary material, which is available to authorized users. Dr. Ryan and Dr. McManus are joint senior authors.

Published
2008

34. UEG899225 Supplemental Material - Supplemental material for Prevalence of coexisting autoimmune thyroidal diseases in coeliac disease is decreasing

Author

Castro, Patricia Dominguez, Harkin, Grace, Hussey, Mary, Christopher, Brian, Kiat, Clifford, Chin, Jun Liong, Trimble, Valerie, McNamara, Deirdre, Padraic MacMathuna, Egan, Brian, Ryan, Barbara, Kevans, David, Abuzakouk, Mohamed, Farrell, Richard, Feighery, Con, Byrnes, Valerie, Mahmud, Nasir, and McManus, Ross

Subjects
FOS: Clinical medicine, FOS: Biological sciences, 111199 Nutrition and Dietetics not elsewhere classified, FOS: Health sciences, 110308 Geriatrics and Gerontology, 69999 Biological Sciences not elsewhere classified, 111299 Oncology and Carcinogenesis not elsewhere classified
Abstract

Supplemental material, UEG899225 Supplemental Material for Prevalence of coexisting autoimmune thyroidal diseases in coeliac disease is decreasing by Patricia Dominguez Castro, Grace Harkin, Mary Hussey, Brian Christopher, Clifford Kiat, Jun Liong Chin, Valerie Trimble, Deirdre McNamara, Padraic MacMathuna, Brian Egan, Barbara Ryan, David Kevans, Mohamed Abuzakouk, Richard Farrell, Con Feighery, Valerie Byrnes, Nasir Mahmud and Ross McManus in United European Gastroenterology Journal

Published
2020
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35. Interleukin 6 predicts increased neural response during face processing in a sample of individuals with schizophrenia and healthy participants: A functional magnetic resonance imaging study

Author

Mothersill, David, primary, King, Sinead, additional, Holleran, Laurena, additional, Dauvermann, Maria, additional, Patlola, Saahithh, additional, Rokita, Karolina, additional, McManus, Ross, additional, Keynon, Marcus, additional, McDonald, Colm, additional, Hallahan, Brian, additional, Corvin, Aiden, additional, Morris, Derek, additional, Kelly, John, additional, McKernan, Declan, additional, and Donohoe, Gary, additional

Published
2021
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36. Variants in RUNX3 Contribute to Susceptibility to Psoriatic Arthritis, Exhibiting Further Common Ground With Ankylosing Spondylitis

Author

Apel, Maria, Uebe, Steffen, Bowes, John, Giardina, Emiliano, Korendowych, Eleanor, Juneblad, Kristina, Pasutto, Francesca, Ekici, Arif B., McManus, Ross, Ho, Pauline, Bruce, Ian N., Ryan, Anthony W., Behrens, Frank, Böhm, Beate, Traupe, Heiko, Lohmann, Jörg, Gieger, Christian, Wichmann, Heinz-Erich, Padyukov, Leonid, FitzGerald, Oliver, Alenius, Gerd-Marie, McHugh, Neil J., Novelli, Giuseppe, Burkhardt, Harald, Barton, Anne, Reis, André, and Hüffmeier, Ulrike

Published
2013
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45. Meta-analysis of genome-wide association studies in celiac disease and rheumatoid arthritis identifies fourteen non-HLA shared loci

Author

Zhernakova, Alexandra, Stahl, Eli A, Trynka, Gosia, Raychaudhuri, Soumya, Festen, Eleanora, Franke, Lude, Fehrmann, Rudolf S N, Kurreeman, Fina A S, Thomson, Brian, Gupta, Namrata, Romanos, Jihane, McManus, Ross, Ryan, Anthony W, Turner, Graham, Remmers, Elaine F, Greco, Luigi, Toes, Rene, Grandone, Elvira, Mazzilli, Maria Cristina, Rybak, Anna, Cukrowska, Bozena, Li, Yonghong, de Bakker, Paul I W, Gregersen, Peter K, Worthington, Jane, Siminovitch, Katherine A, Klareskog, Lars, Huizinga, Tom W J, Wijmenga, Cisca, and Plenge, Robert M

Published
2011
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47. Prevalence of coexisting autoimmune thyroidal diseases in coeliac disease is decreasing

Author

Castro, Patricia Dominguez, primary, Harkin, Grace, additional, Hussey, Mary, additional, Christopher, Brian, additional, Kiat, Clifford, additional, Chin, Jun Liong, additional, Trimble, Valerie, additional, McNamara, Deirdre, additional, MacMathuna, Padraic, additional, Egan, Brian, additional, Ryan, Barbara, additional, Kevans, David, additional, Abuzakouk, Mohamed, additional, Farrell, Richard, additional, Feighery, Con, additional, Byrnes, Valerie, additional, Mahmud, Nasir, additional, and McManus, Ross, additional

Published
2020
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