期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 40, 期 2, 页码 548-558出版社
WILEY
DOI: 10.1002/eji.200939886
关键词
Galectin-9; Immune suppression; Lung; Macrophage; Pneumonitis
类别
资金
- Japan Society for Promotion of Science (JSPS) [(13) 2008-2009 (20790570)]
- Kagawa University Characteristic Prior Research Fund
- Japanese Ministry of Education, Culture, Sports, Science, and Technology
Galectin-9 (Gal-9) plays pivotal roles in the modulation of innate and adaptive immunity to suppress T-cell-mediated autoimmune models. However, it remains unclear if Gal-9 plays a suppressive role for T-cell function in non-autoimmune disease models. We assessed the effects of Gal-9 on experimental hypersensitivity pneumonitis induced by Trichosporon asahii. When Gal-9 was given subcutaneously to C57BL/6 mice at the time of challenge with I asahii, it significantly suppressed T asahii-induced lung inflammation, as the levels of IL-1, IL-6, IFN-gamma, and IL-17 were significantly reduced in the BALF of Gal-9-treated mice. Moreover, co-culture of anti-CD3-stimulated CD4 T cells with BALF cells harvested from Gal-9-treated mice on day 1 resulted in diminished CD4 T-cell proliferation and decreased levels of IFN-gamma and IL-17. CD11b(+) Ly-6C(high)F4/80(+) BALF M( expanded by Gal-9 were responsible for the suppression. We further found in vitro that Gal-9, only in the presence of T asahii, expands CD11b(+)Ly-6C(high)F4/80(+) cells from BM cells, and the cells suppress T-cell proliferation and IFN-gamma and IL-17 production. The present results indicate that Gal-9 expands immunosuppressive CD11b(+)Ly-6C(high) M phi to ameliorate Th1/Th17 cell-mediated hypersensitivity pneumonitis.
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