Methods. Genotype data collected for HLA-DR and 386 microsatellite markers were subjected to multipoint nonparametric linkage analysis. Following analysis of the entire set of families, additional analyses were performed after a priori stratification by disease onset type, age at onset, disease course, and selected HLA-DRB1 alleles. Conclusion. These data support the hypothesis that multiple genes, including at least 1 in the HLA region, influence susceptibility to JRA. These findings for JRA are consistent with findings for other autoimmune diseases and support the notion that common genetic regions contribute to an autoimmune phenotype.Collectively, the varied conditions that constitute juvenile rheumatoid arthritis (JRA) represent the most common chronic rheumatic inflammatory conditions of childhood. Current estimates indicate that as many as 50,000 children in the US have been diagnosed with some form of JRA (1). The diagnosis of JRA is complicated by the heterogeneous nature of the clinical phenotypes and has broadly been defined by the American College of Rheumatology (ACR) (2) based on systemic involvement (fevers, rash, and involvement of other organ systems besides the musculoskeletal system) and mode of disease onset (pauciarticular [Յ4 joints] versus polyarticular [Ն5 joints]).Evidence suggests that JRA is a complex genetic disorder that is influenced by multiple genetic and environmental factors. The sibling risk ratio for a full sibling of a child with JRA is estimated to be 15 (3). These results are consistent with other autoimmune disorders, such as type 1 diabetes (4).

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