CD1d-restricted NKT cell activation enhanced homeostatic proliferation of CD8+ T cells in a manner dependent on IL-4

CD1d-restricted NKT cells are activated by TCR-mediated stimulation via CD1d plus lipid antigens such as alpha-galactosylceramide (α-GalCer). These cells suppressed autoimmunity and graft rejection, but sometimes enhanced resistance to infection and tumor immunity. This double-action phenomenon of N...

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Bibliographic Details
Published in:International immunology 2006-09, Vol.18 (9), p.1397-1404
Main Authors: Ueda, Naoko, Kuki, Hiroko, Kamimura, Daisuke, Sawa, Shinichiro, Seino, Kenichiro, Tashiro, Takuya, Fushuku, Ken-ichi, Taniguchi, Masaru, Hirano, Toshio, Murakami, Masaaki
Format: Article
Language:English
Subjects:
Animals
Antigens, CD1 - immunology
Antigens, CD1 - metabolism
Antigens, CD1d
CD4-Positive T-Lymphocytes - drug effects
CD4-Positive T-Lymphocytes - immunology
CD4-Positive T-Lymphocytes - metabolism
CD8+ T cells
CD8-Positive T-Lymphocytes - drug effects
CD8-Positive T-Lymphocytes - immunology
CD8-Positive T-Lymphocytes - metabolism
Cell Proliferation - drug effects
Galactosylceramides - pharmacology
Homeostasis
homeostatic proliferation
IL-4
Interleukin-4 - immunology
Interleukin-4 - metabolism
Killer Cells, Natural - immunology
Killer Cells, Natural - metabolism
Lymphocyte Activation - immunology
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Knockout
NKT cells
STAT6 Transcription Factor - immunology
STAT6 Transcription Factor - metabolism
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Summary:CD1d-restricted NKT cells are activated by TCR-mediated stimulation via CD1d plus lipid antigens such as alpha-galactosylceramide (α-GalCer). These cells suppressed autoimmunity and graft rejection, but sometimes enhanced resistance to infection and tumor immunity. This double-action phenomenon of NKT cells is partly explained by cytokines produced by NKT cells. Therefore, roles of cytokines from activated NKT cells have been extensively examined; however, their roles on T cell homeostatic proliferation in lymphopenic condition have not been investigated. Here, we showed that α-GalCer enhanced homeostatic proliferation of CD8+ but not CD4+ T cells and this effect of α-GalCer was required for NKT cells. IL-4 was essential and sufficient for this NKT cell action on CD8+ T cell homeostatic proliferation. Importantly, the expression of IL-4Rα and STAT6 in CD8+ T cells was essential for the NKT activity, indicating a direct action of IL-4 on CD8+ T cells. Consistent with this, the level of IL-4Rα expression on memory phenotype CD8+ T cells was higher than that on naive phenotype one and CD4+ T cells. Thus, these results showed the ‘involvement’ of IL-4 that is produced from activated NKT cells for CD8+ T cell homeostatic proliferation in vivo.
ISSN:0953-8178
1460-2377
DOI:10.1093/intimm/dxl073