Studies in the pathogenesis of rheumatoid arthritis. 1: Immunogenetic associations

The critical role of CMI in the pathogenesis of RA has been reinforced, if not entirely illuminated, by recent information about the immunogenetic basis for individual susceptibility, in regard to genes of the HLA-D locus that control expression of MHC II determinants. An aberration in the T-cell response to cells presenting antigen is strongly implied, and must therefore be characterized. We will need to know what types of antigen trigger aberrant responses in those that are susceptible, and whether continuous presence of antigen is necessary to sustain chronic inflammation. The second part of this article will review immunological injury to joint tissues as an off-shoot of the CMI and HI responses of RA. Using data from animal models we shall examine criteria for establishing chronic joint inflammation, and consider their relevance to RA. We shall also consider the problem of why some joints are more susceptible than others to immunological injury.