Juvenile chronic arthritis covers a heterogeneous group of arthritides for which there appears to be a genetically determined susceptibility. The exact events which trigger or perpetuate an arthritic disease have yet to be defined. There is circumstantial clinical evidence that JCA can be initiated by environmental factors such as infection, and indirect laboratory evidence that immune responses to infectious agents are associated with ongoing JCA; such immune responses seem particularly vigorous within the joint space. Although the weight of evidence favours the hypothesis that the intra-articular inflammatory process is antigen-driven, none of the critical antigens have been identified, and it is still unclear whether they are derived from infectious agents or are true auto-antigens. We can however expect progress to be made, since techniques are now available for defining the antigenic specificity and TCR usage of synovial T cell populations, while PCR allows exquisitely sensitive detection of infectious agents deposited in the synovial space. Application of these techniques should lead to an enhanced understanding of whether (or in what circumstances) infectious agents are involved in the pathogenesis of arthritis in children.