中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
High doses of alpha-galactosylceramide potentiate experimental autoimmune encephalomyelitis by directly enhancing th17 response

文献类型:期刊论文

作者Qian, Gaochao2; Qin, Xia2; Zang, Ying Qin3; Ge, Baoxue1; Guo, Taylor B.1; Wan, Bing1; Fang, Lei1; Zhang, Jingwu Z.1
刊名Cell research
出版日期2010-04-01
卷号20期号:4页码:480-491
关键词Alpha-gc Experimental autoimmune encephalomyelitis Il-17
ISSN号1001-0602
DOI10.1038/cr.2010.6
通讯作者Zhang, jingwu z.(jwzang@sibs.ac.cn)
英文摘要Alpha-galactosylceramide (alpha-gc) is widely known to activate invariant natural killer t (inkt) cells to suppress myelin antigen-specific th1 responses, protecting susceptible mice against experimental autoimmune encephalomyelitis (eae). here, we demonstrate an unexpected finding that high doses of alpha-gc exacerbated, rather than ameliorated, eae. similar results were observed when mog(35-55)-specific t cells treated with high-dose alpha-gc were transferred into naive syngeneic recipient mice. further study showed that high doses of alpha-gc directly enhance the th17 and th1 response by activation of cd4(+)cd44(+) memory t cells through phosphorylation of stat3 and activation of nf-kappa b. unlike the activation of inkt cells by low doses of alpha-gc, high doses of alpha-gc directly interacted with cd1d expressed on t cells and activated th17 and th1 cells. furthermore, antigen-presenting cells (apcs) predominantly express cd1d1, whereas the majority of cd4(+) t cells express cd1d2. knockdown of cd1d1 or cd1d2 gene expression by rnai interfered with the activation of inkt or th17/th1 cells, respectively. therefore, alpha-gc treatment could improve or worsen eae by engaging either apcs or th17/th1 cells depending on the dose used.
WOS关键词KILLER T-CELLS ; ANTIGEN-PRESENTING MOLECULES ; INVARIANT NKT CELLS ; AIRWAY HYPERREACTIVITY ; INDUCED ARTHRITIS ; CD1 MOLECULES ; PRODUCE IL-17 ; CUTTING EDGE ; MOUSE CD1 ; ACTIVATION
WOS研究方向Cell Biology
WOS类目Cell Biology
语种英语
WOS记录号WOS:000276838100011
出版者INST BIOCHEMISTRY & CELL BIOLOGY
URI标识http://www.irgrid.ac.cn/handle/1471x/2411441
专题中国科学院大学
通讯作者Zhang, Jingwu Z.
作者单位1.Chinese Acad Sci, Grad Sch, Shanghai Inst Biol Sci, Inst Hlth Sci, Shanghai 200031, Peoples R China
2.Shanghai Jiao Tong Univ, Sch Med, Shanghai Inst Immunol, Shanghai 200025, Peoples R China
3.Chinese Acad Sci, Grad Sch, Shanghai Inst Biol Sci, Inst Nutr Sci, Shanghai 200031, Peoples R China
推荐引用方式
GB/T 7714
Qian, Gaochao,Qin, Xia,Zang, Ying Qin,et al. High doses of alpha-galactosylceramide potentiate experimental autoimmune encephalomyelitis by directly enhancing th17 response[J]. Cell research,2010,20(4):480-491.
APA Qian, Gaochao.,Qin, Xia.,Zang, Ying Qin.,Ge, Baoxue.,Guo, Taylor B..,...&Zhang, Jingwu Z..(2010).High doses of alpha-galactosylceramide potentiate experimental autoimmune encephalomyelitis by directly enhancing th17 response.Cell research,20(4),480-491.
MLA Qian, Gaochao,et al."High doses of alpha-galactosylceramide potentiate experimental autoimmune encephalomyelitis by directly enhancing th17 response".Cell research 20.4(2010):480-491.

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来源:中国科学院大学

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