The immunopathogenic mechanisms of juvenile rheumatoid arthritis (JRA) have been debated. A possible cellular-mediated hypothesis versus a possible B cell hyperreactivity have been entertained. This review will focus on some recent cellular work in JRA and also further evaluation of cytokine levels and their role in inflammation in JRA. Recent studies have evaluated the interrelationship of Th1/Th2 immune responses in the immunopathogenesis of JRA, and their effect on cytokine release. Studies have indicated a pro-inflammatory response in systemic-onset JRA manifested by increased secretion of interleukin-6, whereas an anti-inflammatory response has been noted by increases of IL-4 mRNA and IL-10 mRNA in pauciarticular-onset JRA. The continued finding of elevated levels of tumor necrosis factor-alpha (TNF-alpha) and its receptors in association with inflammatory activity has been seen. The recent use of a TNF fusion protein to block TNF-alpha activity in JRA has further contributed to this finding. Further studies on specific cytokines will be helpful in the future in trying to determine the different roles cytokines play in JRA subtypes and would contribute to the development of better therapeutic regimens.