Emerging Tim-3 functions in antimicrobial and tumor immunity

被引：240

作者：

Sakuishi, Kaori ^{[1
]}

Jayaraman, Pushpa ^{[2
]}

Behar, Samuel M. ^{[2
]}

Anderson, Ana C. ^{[1
]}

Kuchroo, Vijay K. ^{[1
]}

机构：

[1] Harvard Univ, Sch Med, Ctr Neurol Dis, Brigham & Womens Hosp, Boston, MA 02115 USA

[2] Harvard Univ, Sch Med, Div Rheumatol, Brigham & Womens Hosp, Boston, MA 02115 USA

来源：

TRENDS IN IMMUNOLOGY | 2011年 / 32卷 / 08期

关键词：

T-CELL EXHAUSTION; CHRONIC VIRAL-INFECTION; MULTIPLE INHIBITORY RECEPTORS; MEDIATED ANTITUMOR IMMUNITY; C VIRUS-INFECTION; APOPTOTIC CELLS; PD-1; EXPRESSION; DISEASE PROGRESSION; MELANOMA PATIENTS; RESPONSES;

D O I：

10.1016/j.it.2011.05.003

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

T cell immunoglobulin-3 (Tim-3) has been identified as a marker of differentiated interferon-gamma-producing CD4(+) T helper type 1 and CD8(+) T cytotoxic type 1 cells. The interaction of Tim-3 with its ligand, galectin-9 (Gal-9), induces cell death, and in vivo blockade of this interaction results in exacerbated autoimmunity and abrogation of tolerance in experimental models, establishing Tim-3 as a negative regulatory molecule. Recent studies have uncovered additional mechanisms by which Tim-3 negatively regulates T cell responses, such as promoting the development of CD8+ T cell exhaustion and inducing expansion of myeloid-derived suppressor cells. In contrast to this inhibitory effect on T cells, Tim-3-Gal-9 interaction promotes macrophage clearance of intracellular pathogens. Here, we focus on the emerging role for Tim-3 in tumor and antimicrobial immunity.

引用

页码：345 / 349

页数：5

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