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- W4313335908 abstract "Abstract γδ T cells are early recruited into mycobacterial lesions. Upon microbial Ag recognition, γδ cells secrete cytokines and chemokines and undergo apoptosis via CD95/CD95 ligand (CD95L) interaction, possibly influencing the outcome of infection and the characteristics of the disease. In this paper we show that activated phagocytes acquire, upon challenge with Mycobacterium tuberculosis, the ability to inhibit M. tuberculosis-induced γδ cell apoptosis. Apoptosis protection was due to NO because it correlated with NO synthase (NOS)-2 induction and activity in scavenger cells and was abrogated by NOS inhibitors. Furthermore, the NO donor S-nitrosoacetylpenicillamine mimicked the effect of enzyme induction. NO left unaffected the expression of CD95 and CD95L, suggesting interference with an event ensuing CD95/CD95L interaction. NO was found to interfere with the intracellular accumulation of ceramide and the activation of caspases, which were involved in γδ T cells apoptosis after M. tuberculosis recognition. We propose that NO generated by infected macrophages determines the life span and therefore the function of lymphocytes at the infection site, thus linking innate and adaptive immunity." @default.
- W4313335908 created "2023-01-06" @default.
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- W4313335908 date "1999-08-01" @default.
- W4313335908 modified "2023-10-11" @default.
- W4313335908 title "Generation of Nitric Oxide by the Inducible Nitric Oxide Synthase Protects γδ T Cells from<i>Mycobacterium tuberculosis-</i>Induced Apoptosis" @default.
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- W4313335908 doi "https://doi.org/10.4049/jimmunol.163.3.1570" @default.
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