Two signaling pathways can lead to Fas ligand expression in CD8+ cytotoxic T lymphocyte clones

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Item Type:	Article
Title:	Two signaling pathways can lead to Fas ligand expression in CD8+ cytotoxic T lymphocyte clones
Creators Name:	Anel, A., Simon, A.K., Auphan, N., Buferne, M., Boyer, C., Golstein, P. and Schmitt-Verhulst, A.M.
Abstract:	As shown previously, a given cytotoxic T lymphocyte (CTL) clone (KB5.C20) could be induced to express the Fas ligand (FasL) by either T cell receptor (TCR) engagement or phorbol 12-myristate 13-acetate (PMA)/ionomycin stimulation. In contrast, another CTL clone (BM3.3) has now been found to exert Fas-based cytotoxicity only after TCR engagement, but not after PMA/ionomycin stimulation. This suggested the existence of a PMA-insensitive, antigen-induced pathway leading to FasL expression. The inability of PMA to promote Fas-based cytotoxicity in BM3.3 cells was correlated with a defect in expression of the classical protein kinase C (PKC) isoforms alpha and beta I. In KB5.C20 cells depleted of PMA-sensitive PKC isoforms and thus no longer responsive to PMA, Fas-based cytotoxicity could still be induced via the TCR/CD3 pathway. On the other hand, a requirement for phosphatidylinositol-3 kinase (PI3K) selectively in this TCR/CD3-induced pathway was demonstrated by specific inhibition with wortmannin. These results suggest that FasL expression when induced via the TCR/CD3 involves PI3K, and when induced by PMA/ionomycin requires the expression of PMA-sensitive PKC isoforms absent in clone BM3.3. Additional data suggest that in neither case was NF-kappa B activation implicated in FasL expression.
Keywords:	Fas Ligand, Protein Kinase C Isoforms, Nuclear Factor-xB, Animals, Mice
Source:	European Journal of Immunology
ISSN:	0014-2980
Publisher:	Wiley
Volume:	25
Number:	12
Page Range:	3381-7
Date:	December 1995
Official Publication:	https://doi.org/10.1002/eji.1830251227
PubMed:	View item in PubMed

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