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.
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Authors | H Tsunobuchi, H Nishimura, F Goshima, T Daikoku, Y Nishiyama, Y Yoshikai |
Journal | Journal of immunology (Baltimore, Md. : 1950)
(J Immunol)
Vol. 165
Issue 8
Pg. 4552-60
(Oct 15 2000)
ISSN: 0022-1767 [Print] United States |
PMID | 11035096
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Interleukin-15
- Interleukin-2
- Receptors, Interleukin-2
- Interferon-gamma
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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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