Abstract：
:T-cell receptor-induced apoptosis regulates immune responses and can result from interactions between Fas (Apo1/CD95) and Fas ligand (FasL). Mutations in the genes for Fas and FasL cause disorders resembling human autoimmune diseases in lpr and gld mice, respectively. However, peripheral T-cell deletion takes place in lpr mice, and autoimmune syndromes occur in mouse strains without Fas or FasL defects. Here we show that tumour necrosis factor (TNF) can mediate mature T-cell receptor-induced apoptosis through the p75 TNF receptor. Blockage of both TNF and FasL is required to abrogate T-cell death and TNF mediates the death of most CD8+ T cells, whereas FasL mediates the death of most CD4+ T cells. Our results suggest that autoregulatory apoptosis of the mature T cells can occur by two distinct molecular mechanisms.
journal_name
Naturejournal_title
Natureauthors
Zheng L,Fisher G,Miller RE,Peschon J,Lynch DH,Lenardo MJdoi
10.1038/377348a0subject
Has Abstractpub_date
1995-09-28 00:00:00pages
348-51issue
6547eissn
0028-0836issn
1476-4687journal_volume
377pub_type
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