Interleukin-1 alpha, interleukin-2, and soluble interleukin-2 receptors in polymyositis.
Cell-mediated immunity has been implicated in the pathogenesis of polymyositis (PM). We conducted a prospective study in which serum levels of soluble interleukin-2 receptors (IL-2R), IL-1 alpha, and IL-2 were correlated with creatine kinase (CK) levels and clinical disease activity. Cytokines and IL-2R were quantitated in 133 serum samples from 14 patients by use of an enzyme-linked immunosorbent assay. In patients with acute PM (9 patients), soluble IL-2R and IL-1 alpha levels were elevated initially, but declined rapidly with therapy. A significant linear relationship was found between soluble IL-2R levels and CK levels. IL-2 was initially detectable in only 3 patients, and it disappeared with therapy in all 3. The levels of cytokines and IL-2R were consistently normal in patients with inactive PM (2 patients). In patients with chronic PM (3 patients), the cytokines and soluble IL-2R levels were normal despite persistently abnormal CK levels and/or muscle weakness. Cellular IL-2R levels correlated positively with serum levels of soluble IL-2R. Our studies substantiate a pathogenic role for cellular immunity in PM, with the finding of activation of lymphocytes. The finding of increased levels of IL-1 alpha demonstrates for the first time that there is monocyte activation in PM. Persistent elevation of CK levels after normalization of the levels of cytokines and IL-2R may be prognostic of impending chronic disease. Serum soluble IL-2R appear to be a sensitive indicator of improvement or exacerbation of disease activity in patients with PM.
Wolf
R E
RE
Department of Medicine, Louisiana State University Medical Center, Shreveport 71130.
Baethge
B A
BA
D000328:Adult; D000368:Aged; D005260:Female; D006801:Humans; D007111:Immunity, Cellular; D007375:Interleukin-1 / Q000032:analysis; D007376:Interleukin-2 / Q000032:analysis*; D008297:Male; D008875:Middle Aged; D009220:Myositis / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D015375:Receptors, Interleukin-2 / Q000032:analysis*
D007375:Interleukin-1; D007376:Interleukin-2; D015375:Receptors, Interleukin-2