https://scholars.lib.ntu.edu.tw/handle/123456789/416273
標題: | Galectin-3 negatively regulates dendritic cell production of IL-23/IL-17-axis cytokines in infection by Histoplasma capsulatum | 作者: | Wu, Sheng-Yang Yu, Jhang-Sian Liu, Fu-Tong SHI-CHUEN MIAW Wu-Hsieh, Betty A |
公開日期: | 1-四月-2013 | 出版社: | AMER ASSOC IMMUNOLOGISTS | 卷: | 190 | 期: | 7 | 起(迄)頁: | 3427 | 來源出版物: | Journal of immunology (Baltimore, Md. : 1950) | 摘要: | Galectin-3 (gal3) is known for its immunoregulatory functions in infectious, autoimmune, and inflammatory diseases. However, little is known about its regulatory role in the host's IL-17A response to infection. Using a mouse model of histoplasmosis in which both Th1 and Th17 responses contribute to fungal clearance, we investigated how gal3 regulates IL-17A responses. Our study showed that Histoplasma infection induced gal3(-/-) dendritic cells to produce significantly higher levels of IL-23, TGF-β1, and IL-1β than did gal3(+/+) cells. Infected by the same inoculum of Histoplasma, gal3(-/-) mice had lower fungal burden and produced higher levels of IL-23/IL-17-axis cytokines and lower levels of IL-12 and IFN-γ. Additionally, there was an increase in Th17 cells and a reduction in Th1 cells in infected gal3(-/-) mice. In vitro Th1/Th17-skewing experiments excluded the intrinsic effect of gal3 on Th cell differentiation. Although neutrophils from both gal3(+/+) and gal3(-/-) mice produced IL-17A upon IL-23 stimulation, their contribution to IL-17A production was greater in gal3(-/-) mice than in gal3(+/+) mice. Compared with gal3(+/+) dendritic cells, adoptive transfer of gal3(-/-) dendritic cells resulted in production of significantly higher levels of IL-17-axis cytokines and reduced fungal burden. It appears that reduced fungal burden and preferential IL-17A response in gal3(-/-) mice by both Th17 cells and neutrophils were the result of preferential production of IL-23/IL-17-axis cytokines by dendritic cells. Our study showed that gal3 negatively regulates IL-17A responses through inhibition of IL-23/IL-17-axis cytokine production by dendritic cells. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-84875442417&doi=10.4049%2fjimmunol.1202122&partnerID=40&md5=f597219b32b10940eed26331966b61ec https://scholars.lib.ntu.edu.tw/handle/123456789/416273 |
ISSN: | 0022-1767 | DOI: | 10.4049/jimmunol.1202122 |
顯示於: | 免疫學研究所 |
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