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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

Cited 34 times inthomson ciCited 39 times inthomson ci
Title
Role of CD44 in activation-induced cell death: CD44-deficient mice exhibit enhanced T cell response to conventional and superantigens
Author
McKallip, RJDo, YoonkyungFisher, MTRobertson, JLNagarkatti, PSNagarkatti, M
Keywords
Apoptosis; Cell surface molecules; Transgenic/knockout
Issue Date
2002-09
Publisher
OXFORD UNIV PRESS
Citation
INTERNATIONAL IMMUNOLOGY, v.14, no.9, pp.1015 - 1026
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.
URI
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DOI
10.1093/intimm/dxf068
ISSN
0953-8178
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BME_Journal Papers
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