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Dual effects of Sprouty1 on TCR signaling depending on the differentiation state of the T cell

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dc.contributor.authorChoi, Heon Sik-
dc.contributor.authorCho, Sung Yup-
dc.contributor.authorSchwartz, Ronald H.-
dc.contributor.authorChoi, Kyung Ho-
dc.date.accessioned2024-05-20T07:30:37Z-
dc.date.available2024-05-20T07:30:37Z-
dc.date.created2024-05-20-
dc.date.created2024-05-20-
dc.date.issued2006-05-
dc.identifier.citationJournal of Immunology, Vol.176 No.10, pp.6034-6045-
dc.identifier.issn0022-1767-
dc.identifier.urihttps://hdl.handle.net/10371/203548-
dc.description.abstractSprouty (Spry) is known to be a negative feedback inhibitor of growth factor receptor signaling through inhibition of the Ras/MAPK pathway. Several groups, however, have reported a positive role for Spry involving sequestration of the inhibitory protein c-Cbl. Thus, Spry may have various functions in the regulation of receptor-mediated signaling depending on the context. In the immune system, the function of Spry is unknown. In this study, we investigated the role of Spry1 in T cell activation. Spry1, among the four mammalian homologs, was specifically induced by TCR signaling of CD4(+) murine T cells. In fully differentiated Th1 clones, overexpressed Spry1 inhibited TCR signaling and decreased IL-2 production while reducing expression with specific siRNA transfection had the opposite effect, increasing IL-2 production. In contrast, in naive T cells, Spry1 overexpression enhanced TCR signaling, and increased proliferation and IL-2 production, while siRNA transfection again had the opposite effect, reducing IL-2 production following activation. The enhancing effect in naive cells was abrogated by preactivation of the T cells with Ag and APC, indicating that the history of exposure to Ag is correlated with a hierarchy of T cell responsiveness to Spry1. Furthermore, both the NF-AT and MAPK pathways were influenced by Spry1, implying a different molecular mechanism from that for growth factor receptor signaling. Thus, Spry1 uses a novel mechanism to bring about differential effects on TCR signaling through the same receptor, depending on the differentiation state of the T cell.-
dc.language영어-
dc.publisherAmerican Association of Immunologists-
dc.titleDual effects of Sprouty1 on TCR signaling depending on the differentiation state of the T cell-
dc.typeArticle-
dc.identifier.doi10.4049/jimmunol.176.10.6034-
dc.citation.journaltitleJournal of Immunology-
dc.identifier.wosid000237705200042-
dc.identifier.scopusid2-s2.0-33646488029-
dc.citation.endpage6045-
dc.citation.number10-
dc.citation.startpage6034-
dc.citation.volume176-
dc.description.isOpenAccessY-
dc.contributor.affiliatedAuthorCho, Sung Yup-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.subject.keywordPlusE3 UBIQUITIN LIGASE-
dc.subject.keywordPlusNEGATIVE REGULATION-
dc.subject.keywordPlusANTIGEN RECEPTOR-
dc.subject.keywordPlusCBL-B-
dc.subject.keywordPlusADAPTER PROTEIN-
dc.subject.keywordPlusTYROSINE PHOSPHORYLATION-
dc.subject.keywordPlusPROLIFERATIVE RESPONSE-
dc.subject.keywordPlusDROSOPHILA-SPROUTY-
dc.subject.keywordPlusMAMMALIAN-CELLS-
dc.subject.keywordPlusERK ACTIVATION-
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