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,§
*
William S. Rowe Division of Rheumatology, Children’s Hospital Medical Center, Cincinnati, OH 45229;
Department of Pathology and Laboratory Medicine, University of Cincinnati, Cincinnati, OH 45267;
University of Cincinnati College of Medicine, Cincinnati, OH 45267; and
§
Cincinnati Veterans Administration Medical Center, Cincinnati, OH 45220
IL-2 is generally considered a pro-inflammatory cytokine that
exacerbates Th1-mediated disease states, such as autoimmune arthritis.
Consistent with this role for IL-2, recent studies from our laboratory
demonstrate that IL-2 mRNA is markedly increased during the acute stage
of collagen-induced arthritis (CIA), an animal model of rheumatoid
arthritis. To further define the role of IL-2 in CIA, the levels of
IL-2 protein and its receptor and the effects of IL-2 administration
were analyzed during CIA. IL-2 protein and IL-2R were preferentially
expressed at disease onset, compared with later stages of disease.
Administration of recombinant human IL-2 (rhIL-2) at, or just before,
disease onset exacerbated disease; surprisingly, rhIL-2 given before
disease onset inhibited CIA, associated with reduced cellular and
humoral responses to type II collagen. Determination of in vivo serum
levels of Th1 and Th2 cytokines in response to rhIL-2 treatment
demonstrated that IFN-
, but not IL-4, was markedly up-regulated in
response to IL-2. In mice treated with anti-IFN- Ab, both early
and late IL-2 administration exacerbated CIA. Thus, IL-2 can have two
opposite effects on autoimmune arthritis, a direct stimulatory effect
and an indirect suppressive effect that is mediated by
IFN-.
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