期刊
JOURNAL OF IMMUNOLOGY
卷 164, 期 4, 页码 2233-2239出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.164.4.2233
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- NIAMS NIH HHS [AR42438] Funding Source: Medline
- NIA NIH HHS [AG07996] Funding Source: Medline
This study addresses the effects of IL-1 beta on apoptosis induced by agonistic anti-CD95 (Fas) Ab. IL-1 beta 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-1 beta, indicating that nitric oxide and PGs were not involved in the modulation of CD95-induced apoptosis. However, when the IL-1 beta-dependent induction of NF-kappa B was inhibited, the antiapoptotic effect of IL-1 beta was partially reversed, suggesting that NF-kappa B-mediated gene activation is part of the protective mechanism. In addition, IL-1 beta significantly increased the expression of Bcl-2. The protein tyrosine kinase inhibitor herbimycin A completely eliminated the protective effect of IL-1 beta on CD95-induced apoptosis, These findings suggest that IL-1 beta modulates the CD95 death cascade in chondrocytes by mechanisms that involve tyrosine phosphorylation events and NF-kappa B-dependent gene activation.
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