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DC Field | Value | Language |
---|---|---|
dc.citation.endPage | 1026 | - |
dc.citation.number | 9 | - |
dc.citation.startPage | 1015 | - |
dc.citation.title | INTERNATIONAL IMMUNOLOGY | - |
dc.citation.volume | 14 | - |
dc.contributor.author | McKallip, RJ | - |
dc.contributor.author | Do, Yoonkyung | - |
dc.contributor.author | Fisher, MT | - |
dc.contributor.author | Robertson, JL | - |
dc.contributor.author | Nagarkatti, PS | - |
dc.contributor.author | Nagarkatti, M | - |
dc.date.accessioned | 2023-12-22T11:37:07Z | - |
dc.date.available | 2023-12-22T11:37:07Z | - |
dc.date.created | 2014-10-08 | - |
dc.date.issued | 2002-09 | - |
dc.description.abstract | T cells upon activation are known to up-regulate CD44 expression. However, the precise function of CD44 on activated T cells is not clear. In this report, we demonstrate that signaling through CD44 plays an important role in activation-induced cell death (AICD). CD44 knockout (KO) mice had an elevated in vivo primary and in vitro secondary response to challenge with conalbumin, anti-CD3 mAb and staphylococcal enterotoxin A (SEA), which correlated with reduced AICD when compared to CD44 wild-type mice. In addition, CD44 KO mice exhibited increased delayed-type hypersensitivity response to dinitrofluorobenzene. In a model examining in vitro AICD, splenocytes from CD44 KO mice showed resistance to TCR-mediated apoptosis when compared to splenocytes from CD44 wild-type mice. In addition, signaling through CD44 led to increased apoptosis in TCR-activated but not resting T cells from CD44 wild-type mice without affecting Fas expression. Injection of SEA into mice deficient in CD44 and Fas (CD44 KO/lpr) led to an increased primary response when compared to mice that expressed CD44 but not Fas (CD44 WT/lpr), suggesting that the enhanced response to SEA was dependent on CD44 but not Fas expression. Administration of anti-CD44 mAb into CD44 wild-type mice caused a significant decrease in antigen-specific T cell response. Together, these data implicate CD44 as an important regulator of AICD in T cells. Furthermore, targeting CD44 in vivo may constitute a novel approach to induce apoptosis in activated T cells, and therefore to treat autoimmune diseases, allograft rejection and graft versus host disease. | - |
dc.identifier.bibliographicCitation | INTERNATIONAL IMMUNOLOGY, v.14, no.9, pp.1015 - 1026 | - |
dc.identifier.doi | 10.1093/intimm/dxf068 | - |
dc.identifier.issn | 0953-8178 | - |
dc.identifier.scopusid | 2-s2.0-0036733398 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/7071 | - |
dc.identifier.url | http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0036733398 | - |
dc.identifier.wosid | 000177767100005 | - |
dc.language | 영어 | - |
dc.publisher | OXFORD UNIV PRESS | - |
dc.title | Role of CD44 in activation-induced cell death: CD44-deficient mice exhibit enhanced T cell response to conventional and superantigens | - |
dc.type | Article | - |
dc.description.journalRegisteredClass | scopus | - |
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