STAT3 regulates proliferation and survival of CD8+ T cells: enhances effector responses to HSV-1 infection, and inhibits IL-10+ regulatory CD8+ T cells in autoimmune uveitis.
第一作者:
Cheng-Rong,Yu
第一单位:
Molecular Immunology Section, National Eye Institute, National Institutes of Allergy and Viral Diseases, National Institutes of Health, Building 10, Room 10N109A, 10 Center Drive, Bethesda, MD 20892-1857, USA.
作者:
医学主题词
动物(Animals);细胞凋亡(Apoptosis);自身免疫疾病(Autoimmune Diseases);CD8阳性T淋巴细胞(CD8-Positive T-Lymphocytes);细胞增殖(Cell Proliferation);细胞分离(Cell Separation);流式细胞术(Flow Cytometry);基因表达调控(Gene Expression Regulation);单纯疱疹(Herpes Simplex);疱疹病毒1型, 人(Herpesvirus 1, Human);炎症(Inflammation);白细胞介素10(Interleukin-10);小鼠(Mice);小鼠, 近交C57BL(Mice, Inbred C57BL);小鼠, 基因敲除(Mice, Knockout);表型(Phenotype);STAT3转录因子(STAT3 Transcription Factor);增量调节(Up-Regulation);葡萄膜炎(Uveitis)
DOI
10.1155/2013/359674
PMID
24204098
发布时间
2022-04-09
- 浏览14
Mediators of inflammation
359674页
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