HLA Susceptibility Genes In Rheumatoid Arthritis

Abstract

Rheumatoid arthritis (RA) is an autoimmune condition that results due to the association of both genetic and environmental factors, for instance, smoking and HLA-DRB1. The progression of disease is marked by the onset of autoimmune reactions and mucous membrane inflammation that leads to synovitis, pannus development, as well as the degeneration of cartilages and bones through T cell/B cell and cytokine cross-talks such as tumor necrosis factor-α (TNF-α) and Interleukin 6 (IL-6). While the exact contribution of susceptibility loci to the disease remains unclear, there have been many instances where DRB1 alleles, in addition to other non-HLA loci, affected the predisposition of individuals to disease. Future studies should concentrate on the combination of both epidemiologic and genetic evidence in the framework of current models of arthritogenic pathways. HLA-DRB1 alleles have been identified as some of the major genetic risk factors associated with disease and are responsible for about 30% of the disease genetics. HLA-DRB1 alleles are generally called the “shared epitope” and have considerable links with RA, especially those associated with the presence of ACPA for alleles *04, *01, and *10. There are other HLA settings, including HLA-A, HLA-B, and HLA-DPB1.