The role of HLA-B27 polymorphism and molecular mimicry in spondylarthropathy

Ankylosing spondylitis (AS), reactive arthritis (ReA) and other related spo ndyloarthropathies (SpAs) are characterized by a strong association with th e major histocompatibility complex allele HLA-B27. Experimental evidence fr om humans and transgenic rodents suggests that HLA-B27 is itself involved i n the pathogenesis of SpA. Population and peptide-specificity analysis of H LA-B27 suggest it has a pathogenic function related to antigen presentation . Putative roles for infectious agents have been proposed in ReA and sugges ted in AS. However the mechanism by which HLA-B27 and bacteria interact to induce arthritis is not clear. Molecular mimicry between bacterial epitopes that cross-react with self-B27 peptides is the most persuasive explanation for the pathogenesis of SpA. The experimental studies reviewed here have g reatly increased our knowledge of the structure, function and disease assoc iation of HLA-B27.