The Protective Role of HLA-DRB113 in Autoimmune Diseases
Autoimmune diseases (AIDs) are characterized by a multifactorial aetiology and a complex genetic background, with the MHC region playing a major role. We genotyped for HLA-DRB1 locus 1228 patients with AIDs-213 with Systemic Lupus Erythematosus (SLE), 166 with Psoriasis or Psoriatic Arthritis (Ps +...
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Hindawi Limited
2015-01-01
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Series: | Journal of Immunology Research |
Online Access: | http://dx.doi.org/10.1155/2015/948723 |
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Article |
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DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Andreia Bettencourt Cláudia Carvalho Bárbara Leal Sandra Brás Dina Lopes Ana Martins da Silva Ernestina Santos Tiago Torres Isabel Almeida Fátima Farinha Paulo Barbosa António Marinho Manuela Selores João Correia Carlos Vasconcelos Paulo P. Costa Berta Martins da Silva |
spellingShingle |
Andreia Bettencourt Cláudia Carvalho Bárbara Leal Sandra Brás Dina Lopes Ana Martins da Silva Ernestina Santos Tiago Torres Isabel Almeida Fátima Farinha Paulo Barbosa António Marinho Manuela Selores João Correia Carlos Vasconcelos Paulo P. Costa Berta Martins da Silva The Protective Role of HLA-DRB113 in Autoimmune Diseases Journal of Immunology Research |
author_facet |
Andreia Bettencourt Cláudia Carvalho Bárbara Leal Sandra Brás Dina Lopes Ana Martins da Silva Ernestina Santos Tiago Torres Isabel Almeida Fátima Farinha Paulo Barbosa António Marinho Manuela Selores João Correia Carlos Vasconcelos Paulo P. Costa Berta Martins da Silva |
author_sort |
Andreia Bettencourt |
title |
The Protective Role of HLA-DRB113 in Autoimmune Diseases |
title_short |
The Protective Role of HLA-DRB113 in Autoimmune Diseases |
title_full |
The Protective Role of HLA-DRB113 in Autoimmune Diseases |
title_fullStr |
The Protective Role of HLA-DRB113 in Autoimmune Diseases |
title_full_unstemmed |
The Protective Role of HLA-DRB113 in Autoimmune Diseases |
title_sort |
protective role of hla-drb113 in autoimmune diseases |
publisher |
Hindawi Limited |
series |
Journal of Immunology Research |
issn |
2314-8861 2314-7156 |
publishDate |
2015-01-01 |
description |
Autoimmune diseases (AIDs) are characterized by a multifactorial aetiology and a complex genetic background, with the MHC region playing a major role. We genotyped for HLA-DRB1 locus 1228 patients with AIDs-213 with Systemic Lupus Erythematosus (SLE), 166 with Psoriasis or Psoriatic Arthritis (Ps + PsA), 153 with Rheumatoid Arthritis (RA), 67 with Systemic Sclerosis (SSc), 536 with Multiple Sclerosis (MS), and 93 with Myasthenia Gravis (MG) and 282 unrelated controls. We confirmed previously established associations of HLA-DRB115 (OR = 2.17) and HLA-DRB103 (OR = 1.81) alleles with MS, HLA-DRB103 with SLE (OR = 2.49), HLA-DRB101 (OR = 1.79) and HLA-DRB104 (OR = 2.81) with RA, HLA-DRB107 with Ps + PsA (OR = 1.79), HLA-DRB101 (OR = 2.28) and HLA-DRB108 (OR = 3.01) with SSc, and HLA-DRB103 with MG (OR = 2.98). We further observed a consistent negative association of HLA-DRB113 allele with SLE, Ps + PsA, RA, and SSc (18.3%, 19.3%, 16.3%, and 11.9%, resp., versus 29.8% in controls). HLA-DRB113 frequency in the AIDs group was 20.0% (OR = 0.58). Although different alleles were associated with particular AIDs, the same allele, HLA-DRB113, was underrepresented in all of the six diseases analysed. This observation suggests that this allele may confer protection for AIDs, particularly for systemic and rheumatic disease. The protective effect of HLA-DRB113 could be explained by a more proficient antigen presentation by these molecules, favouring efficient clonal deletion during thymic selection. |
url |
http://dx.doi.org/10.1155/2015/948723 |
work_keys_str_mv |
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doaj-7a125b61c42548c5aadd79b975b6fb8d2020-11-24T23:52:50ZengHindawi LimitedJournal of Immunology Research2314-88612314-71562015-01-01201510.1155/2015/948723948723The Protective Role of HLA-DRB113 in Autoimmune DiseasesAndreia Bettencourt0Cláudia Carvalho1Bárbara Leal2Sandra Brás3Dina Lopes4Ana Martins da Silva5Ernestina Santos6Tiago Torres7Isabel Almeida8Fátima Farinha9Paulo Barbosa10António Marinho11Manuela Selores12João Correia13Carlos Vasconcelos14Paulo P. Costa15Berta Martins da Silva16Immunogenetics Laboratory, Instituto de Ciências Biomédicas Abel Salazar-Universidade do Porto (ICBAS-UP), Rua de Jorge Viterbo Ferreira No. 228, 4050-313 Porto, PortugalImmunogenetics Laboratory, Instituto de Ciências Biomédicas Abel Salazar-Universidade do Porto (ICBAS-UP), Rua de Jorge Viterbo Ferreira No. 228, 4050-313 Porto, PortugalImmunogenetics Laboratory, Instituto de Ciências Biomédicas Abel Salazar-Universidade do Porto (ICBAS-UP), Rua de Jorge Viterbo Ferreira No. 228, 4050-313 Porto, PortugalImmunogenetics Laboratory, Instituto de Ciências Biomédicas Abel Salazar-Universidade do Porto (ICBAS-UP), Rua de Jorge Viterbo Ferreira No. 228, 4050-313 Porto, PortugalImmunogenetics Laboratory, Instituto de Ciências Biomédicas Abel Salazar-Universidade do Porto (ICBAS-UP), Rua de Jorge Viterbo Ferreira No. 228, 4050-313 Porto, PortugalUnit for Multidisciplinary Research in Biomedicine (UMIB), Abel Salazar Institute of Biomedical Sciences (ICBAS), University of Porto (UP), Rua de Jorge Viterbo Ferreira No. 228, 4050-313 Porto, PortugalUnit for Multidisciplinary Research in Biomedicine (UMIB), Abel Salazar Institute of Biomedical Sciences (ICBAS), University of Porto (UP), Rua de Jorge Viterbo Ferreira No. 228, 4050-313 Porto, PortugalUnit for Multidisciplinary Research in Biomedicine (UMIB), Abel Salazar Institute of Biomedical Sciences (ICBAS), University of Porto (UP), Rua de Jorge Viterbo Ferreira No. 228, 4050-313 Porto, PortugalUnit for Multidisciplinary Research in Biomedicine (UMIB), Abel Salazar Institute of Biomedical Sciences (ICBAS), University of Porto (UP), Rua de Jorge Viterbo Ferreira No. 228, 4050-313 Porto, PortugalUnit for Multidisciplinary Research in Biomedicine (UMIB), Abel Salazar Institute of Biomedical Sciences (ICBAS), University of Porto (UP), Rua de Jorge Viterbo Ferreira No. 228, 4050-313 Porto, PortugalUnit for Multidisciplinary Research in Biomedicine (UMIB), Abel Salazar Institute of Biomedical Sciences (ICBAS), University of Porto (UP), Rua de Jorge Viterbo Ferreira No. 228, 4050-313 Porto, PortugalUnit for Multidisciplinary Research in Biomedicine (UMIB), Abel Salazar Institute of Biomedical Sciences (ICBAS), University of Porto (UP), Rua de Jorge Viterbo Ferreira No. 228, 4050-313 Porto, PortugalDepartment of Dermatology, Centro Hospitalar do Porto-Hospital de Santo António (CHP-HSA), Largo Prof. Abel Salazar, 4099-001 Porto, PortugalUnit for Multidisciplinary Research in Biomedicine (UMIB), Abel Salazar Institute of Biomedical Sciences (ICBAS), University of Porto (UP), Rua de Jorge Viterbo Ferreira No. 228, 4050-313 Porto, PortugalUnit for Multidisciplinary Research in Biomedicine (UMIB), Abel Salazar Institute of Biomedical Sciences (ICBAS), University of Porto (UP), Rua de Jorge Viterbo Ferreira No. 228, 4050-313 Porto, PortugalImmunogenetics Laboratory, Instituto de Ciências Biomédicas Abel Salazar-Universidade do Porto (ICBAS-UP), Rua de Jorge Viterbo Ferreira No. 228, 4050-313 Porto, PortugalImmunogenetics Laboratory, Instituto de Ciências Biomédicas Abel Salazar-Universidade do Porto (ICBAS-UP), Rua de Jorge Viterbo Ferreira No. 228, 4050-313 Porto, PortugalAutoimmune diseases (AIDs) are characterized by a multifactorial aetiology and a complex genetic background, with the MHC region playing a major role. We genotyped for HLA-DRB1 locus 1228 patients with AIDs-213 with Systemic Lupus Erythematosus (SLE), 166 with Psoriasis or Psoriatic Arthritis (Ps + PsA), 153 with Rheumatoid Arthritis (RA), 67 with Systemic Sclerosis (SSc), 536 with Multiple Sclerosis (MS), and 93 with Myasthenia Gravis (MG) and 282 unrelated controls. We confirmed previously established associations of HLA-DRB115 (OR = 2.17) and HLA-DRB103 (OR = 1.81) alleles with MS, HLA-DRB103 with SLE (OR = 2.49), HLA-DRB101 (OR = 1.79) and HLA-DRB104 (OR = 2.81) with RA, HLA-DRB107 with Ps + PsA (OR = 1.79), HLA-DRB101 (OR = 2.28) and HLA-DRB108 (OR = 3.01) with SSc, and HLA-DRB103 with MG (OR = 2.98). We further observed a consistent negative association of HLA-DRB113 allele with SLE, Ps + PsA, RA, and SSc (18.3%, 19.3%, 16.3%, and 11.9%, resp., versus 29.8% in controls). HLA-DRB113 frequency in the AIDs group was 20.0% (OR = 0.58). Although different alleles were associated with particular AIDs, the same allele, HLA-DRB113, was underrepresented in all of the six diseases analysed. This observation suggests that this allele may confer protection for AIDs, particularly for systemic and rheumatic disease. The protective effect of HLA-DRB113 could be explained by a more proficient antigen presentation by these molecules, favouring efficient clonal deletion during thymic selection.http://dx.doi.org/10.1155/2015/948723 |