title: 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.
authors.affiliation: Laboratories of. Host Defense and Germfree Life and Virology, Research Institute of Disease Mechanism and Control, Nagoya University School of Medicine, Nagoya, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Tsunobuchi
authors.forename: H
authors.initials: H
authors.lastname: Nishimura
authors.forename: F
authors.initials: F
authors.lastname: Goshima
authors.forename: T
authors.initials: T
authors.lastname: Daikoku
authors.forename: Y
authors.initials: Y
authors.lastname: Nishiyama
authors.forename: Y
authors.initials: Y
authors.lastname: Yoshikai
mesh_terms: D000818:Animals; D001202:Ascitic Fluid / Q000235:genetics / Q000276:immunology / Q000473:pathology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology* / Q000378:metabolism; D002454:Cell Differentiation / Q000235:genetics / Q000276:immunology; D002478:Cells, Cultured; D005260:Female; D005434:Flow Cytometry; D020022:Genetic Predisposition to Disease; D006558:Herpes Genitalis / Q000235:genetics* / Q000276:immunology / Q000517:prevention & control*; D018258:Herpesvirus 2, Human / Q000276:immunology; D007156:Immunologic Memory / Q000235:genetics*; D007274:Injections, Intraperitoneal; D007371:Interferon-gamma / Q000096:biosynthesis; D019409:Interleukin-15 / Q000096:biosynthesis / Q000494:pharmacology; D007376:Interleukin-2 / Q000494:pharmacology; D008213:Lymphocyte Activation / Q000235:genetics; D008212:Lymphocyte Depletion; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D015375:Receptors, Interleukin-2 / Q000172:deficiency* / Q000235:genetics*; D016176:T-Lymphocyte Subsets / Q000276:immunology* / Q000378:metabolism; D018417:Th1 Cells / Q000378:metabolism / Q000473:pathology
chemical_list: D019409:Interleukin-15; D007376:Interleukin-2; D015375:Receptors, Interleukin-2; D007371:Interferon-gamma