It is increasingly clear that IIM disease susceptibility is statistically highly associated with genes at HLA, which likely interact with environmental factors to trigger disease. IIM may be classified by “traditional” subtype (PM, DM and IBM), but classification by myositis-specific/associated antibody (MSA/MAA) status is increasingly advocated, as the differential presence of these antibodies is predictive of an individual’s disease phenotype within the IIM spectrum. Moreover, the MSA/MAA detected in any individual IIM sufferer is predictable from that individual’s genotype at HLA. This close association between HLA genotype and IIM subtype, including MSA/MAA status, suggests that HLA genotype is somehow involved in determining overall IIM phenotype. This may mean that, when an IIM is environmentally triggered, the sufferer’s disease phenotype is somehow predetermined by their genotype status at HLA. The notion that IIM phenotype is linked mechanistically to HLA genes is however speculative, and currently unproven. Recent research has progressed our understanding of immunogenetics, and its potential implications for differential disease expression including circulating autoantibodies in IIM as well as in other autoimmune diseases. The remit of this presentation is to use the results of these recent immunogenetic studies in IIM and other autoimmune diseases to explore the hypothesis that HLA gene:gene and HLA gene:envioronment interactions may play important roles in determining disease susceptibility, phenotype and treatment outcomes in IIM and in other autoimmune diseases.
Disclosure of Interest None Declared