NDLI: Enzymatically active single chain caspase-8 maintains T-cell survival during clonal expansion

Content Provider	PubMed Central
Author	Leverrier, S. Salvesen, G. S. Walsh, C. M.
Copyright Year	2011
Abstract	The extrinsic, or death receptor, pathway integrates apoptotic signals through the protease caspase-8 (casp8). Beyond cell death regulation, non-apoptotic functions of casp8 include its essential requirement for hematopoiesis and lymphocyte clonal expansion, and tempering of autophagy in T cells. However, the mechanistic basis for the control of these disparate cellular processes remains elusive. Here, we show that casp8-deficient T-cell survival was rescued by enzymatically active, but not inactive, casp8-expressing retroviruses. The casp8 catalytic induction in proliferating T cell occurred independent of extrinsic and intrinsic apoptotic-signaling cascades and did not induce casp8 proteolytic processing. Using a biotinylated probe selectively targeting enzymatically active caspases, catalytically active full-length casp8 was found in vivo in dividing T cells. A casp8 D387A processing mutant was able to rescue casp8-deficient T-cell proliferation, validating that casp8 self-processing is not required for its non-apoptotic function(s). Finally, casp8 activity was highest in CD8+ T cells, the most rapidly proliferating subset. These results show that the catalytically competent form of casp8 is required for rapid T-cell proliferation in response to TCR ligation, but that processing of the caspase is only necessary to promote apoptosis.
Related Links	http://dx.doi.org/10.1038/cdd.2010.69
Ending Page	98
Page Count	9
Starting Page	90
File Format	PDF
ISSN	13509047
e-ISSN	14765403
Journal	Cell Death and Differentiation
Issue Number	1
Volume Number	18
Language	English
Publisher	Nature Publishing Group
Publisher Date	2011-01-01
Access Restriction	Open
Rights Holder	Nature Publishing Group
Subject Keyword	Cell Biology Molecular Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cell Biology Molecular Biology

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