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IL-1ß Protects Human Chondrocytes from CD95-Induced Apoptosis¹

Division of Arthritis Research, Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037

This study addresses the effects of IL-1ß on apoptosis induced by agonistic anti-CD95 (Fas) Ab. IL-1ß inhibited anti-CD95 Ab-induced apoptosis in all preparations of normal human articular chondrocytes tested. Inhibitors of nitric oxide synthase or cyclooxygenase did not influence the protective effect of IL-1ß, indicating that nitric oxide and PGs were not involved in the modulation of CD95-induced apoptosis. However, when the IL-1ß-dependent induction of NF-B was inhibited, the antiapoptotic effect of IL-1ß was partially reversed, suggesting that NF-B-mediated gene activation is part of the protective mechanism. In addition, IL-1ß significantly increased the expression of Bcl-2. The protein tyrosine kinase inhibitor herbimycin A completely eliminated the protective effect of IL-1ß on CD95-induced apoptosis. These findings suggest that IL-1ß modulates the CD95 death cascade in chondrocytes by mechanisms that involve tyrosine phosphorylation events and NF-B-dependent gene activation.

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