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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


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

DC Field Value Language McKallip, RJ ko Do, Yoonkyung ko Fisher, MT ko Robertson, JL ko Nagarkatti, PS ko Nagarkatti, M ko 2014-10-10T01:58:26Z - 2014-10-08 ko 2002-09 -
dc.identifier.citation INTERNATIONAL IMMUNOLOGY, v.14, no.9, pp.1015 - 1026 ko
dc.identifier.issn 0953-8178 ko
dc.identifier.uri -
dc.identifier.uri 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 * 2015-05-06 * 2014-10-08 *
dc.identifier.doi 10.1093/intimm/dxf068 ko
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