This review considers the epidemiological aspects of the genetic investigation of rheumatoid arthritis (RA). Problems both of disease definition and disease heterogeneity render studies difficult to undertake and interpret. The selection of individuals both in population and family studies can explain divergent results. Despite the insights into the immunopathogenesis of RA afforded by the demonstration of an association between the disease and HLA class II genes, the latter have only a limited role in explaining differences, both between individuals and between populations, in susceptibility to RA.
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