Interleukin production in juvenile chronic arthritis.

SIR, We read with interest the paper by Gilman and coworkers who showed that in rats with adjuvant-induced arthritis peritoneal macrophages produce higher amounts of interleukin 1 (IL-1), while splenic T cells produce less interleukin 2 (IL-2) than controls.' We found comparable results when studying interleukin production by peripheral blood mononuclear cells in children with juvenile chronic arthritis (JCA) (unpublished data). We investigated a total of 28 children with JCA ranging in age from 3 to 16 years. Ten presented a systemic form, six a polyarticular, and twelve a pauciarticular form. Patients were divided according to clinical activity of the disease into three groups: active disease, partial remission, and remission. Twentyone age matched healthy children served as controls. Peripheral blood monocytes were isolated by adherence and stimulated in vitro with lipopolysaccharide: IL-1 in the supernatants was assessed by a thymocyte coproliferation assay. Peripheral blood lymphocytes were stimulated in vitro with phytohaemagglutinin, and IL-2 in the supernatants was quantified by an IL-2-dependent cell line. Monocytes from patients with JCA produced significantly more IL-1 than controls (17-1±11-1 (SD) v 10-6±8-9 (SD), p<0-05). while lymphocytes from the same patients produced significantly less IL-2 than controls (40-6±31.2 (SD) v 69-8±40 9 (SD), p<0-01). These findings could not be explained by concurrent treatment. The greater IL-1 production was more evident in patients with active disease, whereas production of IL-2 was lowest in patients with complete remission. No major differences were observed among the three JCA subtypes. The similarities between our findings in JCA patients and the findings of Gilman et al.t in adjuvant-induced arthritis suggest that modulation of interleukin production may be of relevance in the pathogenesis of JCA, and, together with the previous finding of reduced production of IL-2 in adult rheumatoid arthritis and systemic lupus erythematosus,2 3 indicates that aberrant regulation of interleukin cascade may be a common feature (probably secondary to different aetiologic factors) of some immunemediated diseases.