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Do, Yoonkyung
DC-based Immune System & Immunotherapy (DISNI) Lab
Research Interests
  • Study on various subsets of dendritic cells and their immunological functions
  • Vaccine development by targeting pathogenic antigens to distinct DC subsets via anti-DC-subset-specific-receptor monoclonal antibodies
  • Characterization of roles of DCs in tumor microenvironment and tumor metastasis
  • Studies on role of DCs in neuro-related diseases
  • Study DCs in collaboration with Biotechnology or Engineering field

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Role of CD44 in activation-induced cell death: CD44-deficient mice exhibit enhanced T cell response to conventional and superantigens

DC Field Value Language
dc.contributor.author McKallip, RJ ko
dc.contributor.author Do, Yoonkyung ko
dc.contributor.author Fisher, MT ko
dc.contributor.author Robertson, JL ko
dc.contributor.author Nagarkatti, PS ko
dc.contributor.author Nagarkatti, M ko
dc.date.available 2014-10-10T01:58:26Z -
dc.date.created 2014-10-08 ko
dc.date.issued 2002-09 -
dc.identifier.citation INTERNATIONAL IMMUNOLOGY, v.14, no.9, pp.1015 - 1026 ko
dc.identifier.issn 0953-8178 ko
dc.identifier.uri https://scholarworks.unist.ac.kr/handle/201301/7071 -
dc.identifier.uri http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0036733398 ko
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. ko
dc.description.statementofresponsibility close -
dc.language ENG ko
dc.publisher OXFORD UNIV PRESS ko
dc.subject Apoptosis ko
dc.subject Cell surface molecules ko
dc.subject Transgenic/knockout ko
dc.title Role of CD44 in activation-induced cell death: CD44-deficient mice exhibit enhanced T cell response to conventional and superantigens ko
dc.type ARTICLE ko
dc.identifier.scopusid 2-s2.0-0036733398 ko
dc.identifier.wosid 000177767100005 ko
dc.type.rims ART ko
dc.description.wostc 34 *
dc.description.scopustc 39 *
dc.date.tcdate 2015-05-06 *
dc.date.scptcdate 2014-10-08 *
dc.identifier.doi 10.1093/intimm/dxf068 ko
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