venile rheumatoid arthritis (JRA) is the most frequent pediatric connective ssue disease. It is still unclear if the disease represents a single tity or several diseases with multiple pathogenetic mechanisms. Among the ssible causes are infection, trauma, stress, immunogenetic predisposition d autoimmunity. The autoimmune nature of the disease has been supported : 1) increased frequency of antinuclear antibodies and rheumatoid factor the sera of these patients, 2) the presence of circulating autoantibodies rected against the T cell subpopulation which induces the generation of ppressor cells, 3) segregation of certain HLA antigens such as HLA-DW5 and A DW-8, and 4) sporadic, not well-documented reports of deficient ripheral immune cell functions. Careful analysis of various cellular munological functions in vitro using modern more sophisticated munological techniques is absolutely needed in order to shed light on the mune status of patients with JRA. jor findings to date include: increased numbers of pre-activated B and T mphocytes in the peripheral blood and altered functions of selected T cell lper and suppressor cell assays. Studies are in progress to identify the thogenesis of these immunoregulatory disturbances and to identify potential ctors which can restore immune function toward normal in JRA patients.
