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Acta Physiologica Congress

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Acta Physiologica 2011; Volume 201, Supplement 682
The 90th Annual Meeting of The German Physiological Society
3/26/2011-3/29/2011
Regensburg, Germany


FAS APOPTOTIC INHIBITORY MOLECULE- 3(FAIM3) /TOSO REGULATES PHENOTYPE, CALCIUM ENTRY UPON TCR ACTIVATION AND PERFORIN EXPRESSION IN CTLS
Abstract number: P323

*Merches1 K., Bhavsar1 S., Bobbala1 D., Schmidt1 S., Lang1 F.

T-lymphocyte (CTL) survival upon activation induced cell death is critically dependent on the expression of anti-apoptotic gene Fas apoptotic inhibitory molecule3 (FAIM3) /TOSO, which plays an important role in IL-2-mediated activation induced cell death (AICD). Down-regulation of TOSO significantly increases susceptibility to apoptosis. The present study explored the role of TOSO in regulation of calcium entry into and function of CD8 T cells. CTLs were cultured from gene trageted TOSO knockout mice (TOSO-/-) and corresponding wildtype mice (TOSO+/+), by stimulating with anti-CD3 for 48h followed by culturing the cells in IL2 supplemented medium for 3 days. The calcium entry upon TCR stimulation was determined by incubating with anti-CD3 followed by cross linking with secondary antibody. As a result, TOSO-/- CTLs show significantly higher calcium entry as compared to TOSO+/+ CTLs. Moreover, the abundance of surface marker CD44 was lower in CD4 and CD8 T cells from TOSO-/- mice than in the respective cells from TOSO+/+ mice. Moreover, perforin expression was significantly lower in TOSO-/- CTLs than in TOSO+/+ CTLs. In conclusion, TOSO is a powerful regulator of T lymphocyte of CD44 and perforin expression as well as calcium entry upon TCR stimulation.

To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 201, Supplement 682 :P323

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