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Memory-type CD8+ T cells protect IL-2 receptor alpha-deficient mice from systemic infection with herpes simplex virus type 2.

Abstract
IL-2Ralpha-deficient (IL-2Ralpha(-/-)) mice exhibit an impaired activation-induced cell death for T cells and develop abnormal T cell activation with age. In our study, we found that IL-2Ralpha(-/-) mice at the age of 5 wk contained an increased number of CD44(+)CD69(-)CD8(+) T cells in lymph nodes, which expressed a high intensity of IL-2Rbeta and vigorously proliferated in response to a high dose of IL-15 or IL-2. The T cells produced a large amount of IFN-gamma in response to IL-15 plus IL-12 in a TCR-independent bystander manner. When IL-2Ralpha(-/-) mice were inoculated i.p. with HSV type 2 (HSV-2) 186 strain, they showed resistance to the infection accompanied by an increased level of serum IL-15. The depletion of CD8(+) T cells by in vivo administration of anti-CD8 mAb rendered IL-2Ralpha(-/-) mice susceptible to HSV-2-induced lethality. These results suggest that memory-type CD8(+) T cells play a novel role in the protection against HSV-2 infection in IL-2Ralpha(-/-) mice.
AuthorsH Tsunobuchi, H Nishimura, F Goshima, T Daikoku, Y Nishiyama, Y Yoshikai
JournalJournal of immunology (Baltimore, Md. : 1950) (J Immunol) Vol. 165 Issue 8 Pg. 4552-60 (Oct 15 2000) ISSN: 0022-1767 [Print] United States
PMID11035096 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Interleukin-15
  • Interleukin-2
  • Receptors, Interleukin-2
  • Interferon-gamma
Topics
  • Animals
  • Ascitic Fluid (genetics, immunology, pathology)
  • CD8-Positive T-Lymphocytes (immunology, metabolism)
  • Cell Differentiation (genetics, immunology)
  • Cells, Cultured
  • Female
  • Flow Cytometry
  • Genetic Predisposition to Disease
  • Herpes Genitalis (genetics, immunology, prevention & control)
  • Herpesvirus 2, Human (immunology)
  • Immunologic Memory (genetics)
  • Injections, Intraperitoneal
  • Interferon-gamma (biosynthesis)
  • Interleukin-15 (biosynthesis, pharmacology)
  • Interleukin-2 (pharmacology)
  • Lymphocyte Activation (genetics)
  • Lymphocyte Depletion
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Receptors, Interleukin-2 (deficiency, genetics)
  • T-Lymphocyte Subsets (immunology, metabolism)
  • Th1 Cells (metabolism, pathology)

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