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Journal of Immunology Research
Volume 2015, Article ID 948723, 6 pages
http://dx.doi.org/10.1155/2015/948723
Research Article

The Protective Role of HLA-DRB113 in Autoimmune Diseases

1Immunogenetics Laboratory, Instituto de Ciências Biomédicas Abel Salazar-Universidade do Porto (ICBAS-UP), Rua de Jorge Viterbo Ferreira No. 228, 4050-313 Porto, Portugal
2Unit 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, Portugal
3Department of Neurology, Centro Hospitalar do Porto-Hospital de Santo António (CHP-HSA), Largo Prof. Abel Salazar, 4099-001 Porto, Portugal
4Unidade de Imunologia Clínica (UIC), Centro Hospitalar do Porto-Hospital de Santo António (CHP-HSA), Largo Prof. Abel Salazar, 4099-001 Porto, Portugal
5Department of Dermatology, Centro Hospitalar do Porto-Hospital de Santo António (CHP-HSA), Largo Prof. Abel Salazar, 4099-001 Porto, Portugal
6Department of Internal Medicine, Centro Hospitalar do Porto-Hospital de Santo António (CHP-HSA), Largo Prof. Abel Salazar, 4099-001 Porto, Portugal
7Instituto Nacional de Saúde Dr. Ricardo Jorge (INSA), Rua Alexandre Herculano No. 321, 4000-055 Porto, Portugal

Received 10 August 2015; Accepted 20 October 2015

Academic Editor: Carlo Perricone

Copyright © 2015 Andreia Bettencourt et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

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.