Regulation of Inflammatory Responses by Oncostatin M

Philip M. Wallace(Bristol-Myers Squibb (United States)), John F. MacMaster(Bristol-Myers Squibb (Germany)), Katherine A. Rouleau(Bristol-Myers Squibb (Germany)), T J Brown(Bristol-Myers Squibb (United States)), James Loy(Bristol-Myers Squibb (Germany)), Karen Donaldson(Bristol-Myers Squibb (United States)), Alan F. Wahl(Bristol-Myers Squibb (United States))
The Journal of Immunology
May 1, 1999
Cited by 114Open Access
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Abstract

Abstract Oncostatin M (OM) is a pleiotropic cytokine produced late in the activation cycle of T cells and macrophages. In vitro it shares properties with related proteins of the IL-6 family of cytokines; however, its in vivo properties and physiological function are as yet ill defined. We show that administration of OM inhibited bacterial LPS-induced production of TNF-α and lethality in a dose-dependent manner. Consistent with these findings, OM potently suppressed inflammation and tissue destruction in murine models of rheumatoid arthritis and multiple sclerosis. T cell function and Ab production were not impaired by OM treatment. Taken together these data indicate the activities of this cytokine in vivo are antiinflammatory without concordant immunosuppression.


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