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KMID : 1161520000040040381
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Animal Cells and Systems
2000 Volume.4 No. 4 p.381 ~ p.388
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Function of nitric oxide in activation-induced cell death of tlymphocytes
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Park Yuk-Pheel
Paik Sang-Gi
Kim Young-Sang
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Abstract
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Using a murine T cell hybridoma, activation?induced cell death (AICD) was studied. As an in vitro model system for the AICD, T cell hybridoma expressing TCR/CD3 complex was incubated onto the immobilized purified anti?CD3 antibody. The immobilized anti?CD3 antibody induced AICD effectively up to 40% At 1?100 μM range of SNP, an exogenous source of nitric oxide (NO), the cell proliferation was not affected, but at 1 mM SNP, cell proliferation was significantly reduced. The AICD of T cell hybridoma was inhibited by exogenous NO at non?cytotoxic concentration. In the cells undergoing AICD, the expressions of caspase?3 and FasL were detected, but not iNOS. Similar result was recognized in the apoptosis induced by dexamethasone, an apoptosis?inducing agent. However, the conversion from the inactive form of caspase?3 (32 kDa) to the active form (17 kDa) was significantly reduced in the cells in AICD induced by anti?CD3 antibody. With the result of increased PARP cleavage in the cells, we propose that another PARP cleavage pathway not involving caspase?3 may function in the anti?CD3 antibody induced AICD in the T cell hybridoma.
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KEYWORD
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AICD, Nitric oxide, Caspase-3, Poly(ADP-ribose) polymerase, T lymphocyte
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