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NF‐κB‐dependent Fas ligand expression

Apoptosis of lymphocytes is triggered by different stimuli through the induced expression of Fas and Fas ligand (FasL). Using T cell activation‐induced Fas/FasL expression as a model system, we observed a differential regulation of the induction of Fas and FasL. cAMP inhibited activation‐induced apoptosis by an effective suppression of TCR‐coupled FasL expres sion. In contrast, cAMP weakly interfered with activation‐induced Fas expression, and the remaining Fas molecules on cAMP‐treated T cells still mediated apoptosis. Among the major transcription elements on the FasL promoter, the activation of NF‐κB, but not of NF‐AT and AP‐1, was suppressed by cAMP. The prominent role of NF‐κB was further demonstrated by a better activation of the FasL promoter and an elevated expression of FasL induced by p65 (RelA) overexpression than those induced by AP‐1 or NF‐AT. Our results demonstrate the essential role of NF‐κB for the expression of the death receptor ligand FasL, and suggest a direct link between NF‐κB activation and the expression of FasL. NF‐κB may be the common mediator in the induction of FasL through TCR activation and by various stress stimuli.