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Article: Cellular FLICE-inhibitory protein is required for T cell survival and cycling

TitleCellular FLICE-inhibitory protein is required for T cell survival and cycling
Authors
Issue Date2005
Citation
Journal of Experimental Medicine, 2005, v. 202, n. 3, p. 405-413 How to Cite?
AbstractFas-associated death domain (FADD) and caspase-8 are key signal transducers for death receptor-induced apoptosis, whereas cellular FLICE-inhibitory protein (cFLIP) antagonizes this process. Interestingly, FADD and caspase-8 also play a role in T cell development and T cell receptor (TCR)-mediated proliferative responses. To investigate the underlying mechanism, we generated cFLIP-deficient T cells by reconstituting Rag-/- blastocysts with cFLIP-deficient embryonic stem cells. These Rag chimeric mutant mice (rcFLIP -/-) had severely reduced numbers of T cells in the thymus, lymph nodes, and spleen, although mature T lymphocytes did develop. Similar to FADD- or caspase-8-deficient cells, rcFLIP -/- T cells were impaired in proliferation in response to TCR stimulation. Further investigation revealed that cFLIP is required for T cell survival, as well as T cell cycling in response to TCR stimulation. Interestingly, some signaling pathways from the TCR complex appeared competent, as CD3 plus CD28 cross-linking was capable of activating the ERK pathway in rcFLIP -/- T cells. We demonstrate an essential role for cFLIP in T cell function. JEM © The Rockefeller University Press.
Persistent Identifierhttp://hdl.handle.net/10722/291745
ISSN
2023 Impact Factor: 12.6
2023 SCImago Journal Rankings: 6.838
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChau, Hien-
dc.contributor.authorWong, Veronica-
dc.contributor.authorChen, Nien Jung-
dc.contributor.authorHuang, Huey Lan-
dc.contributor.authorLin, Wen Jye-
dc.contributor.authorMirtsos, Christine-
dc.contributor.authorElford, Alisha R.-
dc.contributor.authorBonnard, Madeleine-
dc.contributor.authorWakeham, Andrew-
dc.contributor.authorYou-Ten, Annick Itie-
dc.contributor.authorLemmers, Bénédicte-
dc.contributor.authorSalmena, Leonardo-
dc.contributor.authorPellegrini, Marc-
dc.contributor.authorHakem, Razq-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorOhashi, Pamela-
dc.contributor.authorYeh, Wen Chen-
dc.date.accessioned2020-11-17T14:55:01Z-
dc.date.available2020-11-17T14:55:01Z-
dc.date.issued2005-
dc.identifier.citationJournal of Experimental Medicine, 2005, v. 202, n. 3, p. 405-413-
dc.identifier.issn0022-1007-
dc.identifier.urihttp://hdl.handle.net/10722/291745-
dc.description.abstractFas-associated death domain (FADD) and caspase-8 are key signal transducers for death receptor-induced apoptosis, whereas cellular FLICE-inhibitory protein (cFLIP) antagonizes this process. Interestingly, FADD and caspase-8 also play a role in T cell development and T cell receptor (TCR)-mediated proliferative responses. To investigate the underlying mechanism, we generated cFLIP-deficient T cells by reconstituting Rag-/- blastocysts with cFLIP-deficient embryonic stem cells. These Rag chimeric mutant mice (rcFLIP -/-) had severely reduced numbers of T cells in the thymus, lymph nodes, and spleen, although mature T lymphocytes did develop. Similar to FADD- or caspase-8-deficient cells, rcFLIP -/- T cells were impaired in proliferation in response to TCR stimulation. Further investigation revealed that cFLIP is required for T cell survival, as well as T cell cycling in response to TCR stimulation. Interestingly, some signaling pathways from the TCR complex appeared competent, as CD3 plus CD28 cross-linking was capable of activating the ERK pathway in rcFLIP -/- T cells. We demonstrate an essential role for cFLIP in T cell function. JEM © The Rockefeller University Press.-
dc.languageeng-
dc.relation.ispartofJournal of Experimental Medicine-
dc.titleCellular FLICE-inhibitory protein is required for T cell survival and cycling-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1084/jem.20050118-
dc.identifier.pmid16043518-
dc.identifier.pmcidPMC2213079-
dc.identifier.scopuseid_2-s2.0-23744487497-
dc.identifier.volume202-
dc.identifier.issue3-
dc.identifier.spage405-
dc.identifier.epage413-
dc.identifier.isiWOS:000230902100010-
dc.identifier.f10001027306-
dc.identifier.issnl0022-1007-

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