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The Journal of Immunology, 1999, 162: 5547-5555.
Copyright © 1999 by The American Association of Immunologists

Regulation of Inflammatory Responses by Oncostatin M

Philip M. Wallace1,2,*, John F. MacMaster{dagger}, Katherine A. Rouleau{dagger}, T. Joseph Brown*, James K. Loy{dagger}, Karen L. Donaldson3,* and Alan F. Wahl3,*

* Bristol-Myers Squibb Pharmaceutical Research Institute, Seattle, WA 98121; and {dagger} Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, NJ 08543

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-{alpha} 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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