IL-15 is critical for the maintenance and innate functions of self-specific CD8+ T cells

Momoe Itsumi, Yasunobu Yoshikai, Hisakata Yamada

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

IL-15 is a pleiotropic cytokine involved in host defense as well as autoimmunity. IL-15-deficient mice show a decrease of memory phenotype (MP) CD8+ T cells, which develop naturally in naïve mice and whose origin is unclear. It has been shown that self-specific CD8+ T cells developed in male H-Y antigen-specific TCR transgenic mice share many similarities with naturally occurring MP CD8+ T cells in normal mice. In this study, we found that H-Y antigen-specific CD8+ T cells in male but not female mice decreased when they were crossed with IL-15-deficient mice, mainly due to impaired peripheral maintenance. The self-specific TCR transgenic CD8+ T cells developed in IL-15-deficient mice showed altered surface phenotypes and reduced effector functions ex vivo. Bystander activation of the self-specific CD8+ T cells was induced in vivo during infection with Listeria monocytogenes, in which proliferation but not IFN-γ production was IL-15-dependent. These results indicated important roles for IL-15 in the maintenance and functions of selfspecific CD8+ T cells, which may be included in the naturally occurring MP CD8+ T-cell population in naïve normal mice and participate in innate host defense responses.

Original languageEnglish
Pages (from-to)1784-1793
Number of pages10
JournalEuropean Journal of Immunology
Volume39
Issue number7
DOIs
Publication statusPublished - Aug 31 2009

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Interleukin-15
Maintenance
T-Lymphocytes
H-Y Antigen
Phenotype
Listeria monocytogenes
Autoimmunity
Transgenic Mice
Cytokines

All Science Journal Classification (ASJC) codes

  • Immunology
  • Immunology and Allergy

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IL-15 is critical for the maintenance and innate functions of self-specific CD8+ T cells. / Itsumi, Momoe; Yoshikai, Yasunobu; Yamada, Hisakata.

In: European Journal of Immunology, Vol. 39, No. 7, 31.08.2009, p. 1784-1793.

Research output: Contribution to journalArticle

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