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| AUTOCRINE T-CELL SUICIDE MEDIATED BY APO-1/(FAS/CD95) |
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| Author(s): DHEIN J, WALCZAK H, BAUMLER C, DEBATIN KM, KRAMMER PH |
| Source: NATURE Volume: 373 Issue: 6513 Pages: 438-441 Published: FEB 2 1995 |
| Times Cited: 1,406 References: 25 |
| Abstract: THE APO-1/(Fas/CD95) cell surface receptor is a member of the nerve growth factor (NGF)/tumour necrosis factor (TNF) receptor superfamily and mediates apoptosis(1-4). Peripheral activated T cells (ATC) from lymphoproliferation (lpr/lpr) mutant mice that express a reduced number of APO-1 receptors have a defect in T-cell receptor (TCR)-induced apoptosis(5,6). This suggests that TCR-induced apoptosis involves APO-1. We tested this hypothesis in various human T cells: (1) malignant Jurkat cells, (2) an alloreactive T-cell clone (S13), and (3) peripheral ATC. TCR triggering through immobilized anti-CD3 antibodies or Staphylococcus enterotoxin B (SEB) superantigen induced expression of the APO-1 ligand and apoptosis in these cells. Anti-CD3-induced apoptosis of Jurkat cells was demonstrated even in single-cell cultures. In all cases apoptosis was substantially inhibited by blocking anti-APO-1 antibody fragments and soluble APO-I receptor decoys. The APO-1 ligand was found in the supernatant of activated Jurkat cells as a soluble cytokine. We propose that TCR-induced apoptosis in ATC can occur through an APO-1 ligand-mediated autocrine suicide. These results provide a mechanism for suppression of the immune response and for peripheral tolerance by T-cell deletion. |
| Document Type: Article |
| Language: English |
Addresses:
1. GERMAN CANC RES CTR, TUMORIMMUNOL PROGRAM, D-69120 HEIDELBERG, GERMANY
2. UNIV HEIDELBERG, CHILDRENS HOSP, D-69120 HEIDELBERG, GERMANY |
| Publisher: MACMILLAN MAGAZINES LTD, 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF |
| Subject Category: Multidisciplinary Sciences |
| IDS Number: QE670 |
| ISSN: 0028-0836 |
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