TIM-3 in autoimmunity

被引：97

作者：

Anderson, Ana C.

Anderson, David E.

机构：

[1] Brigham & Womens Hosp, Ctr Neurol Dis, Boston, MA 02115 USA

[2] Harvard Univ, Sch Med, Ctr Neurol Dis, Boston, MA 02115 USA

来源：

CURRENT OPINION IN IMMUNOLOGY | 2006年 / 18卷 / 06期

关键词：

D O I：

10.1016/j.coi.2006.09.009

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 and mucin domain (TIM)-3 is a molecule expressed on terminally differentiated murine Th1 cells but not on Th2 cells. Identification of galectin-9 as a ligand for TIM-3 has now firmly established the TIM-3-galectin-9 pathway as an important regulator of Th1 immunity and tolerance induction. TIM-3 is similarly expressed on human Th1 cells and not on Th2 cells, which suggests that TIM-3 might also contribute to Th1 regulation in humans. In addition, genetic data associate the TIM locus and specific TIM-3 polymorphisms with various immune-mediated diseases. Most importantly, recent data suggest a novel paradigm in which dysregulation of the TIM-3-galectin-9 pathway could underlie chronic autoimmune disease states, such as multiple sclerosis.

引用

收藏

页码：665 / 669

页数：5

相关论文

共 29 条

[1]

Butterfield RJ, 1998, J IMMUNOL, V161, P1860

[2] The association of TIM-3 gene polymorphism with atopic disease in Korean population [J].

Chae, SC ;

Park, YR ;

Lee, YC ;

Lee, JH ;

Chung, HT .

HUMAN IMMUNOLOGY, 2004, 65 (12) :1427-1431

[3] The polymorphisms of Th1 cell surface gene Tim-3 are associated in a Korean population with rheumatoid arthritis [J].

Chae, SC ;

Parka, YR ;

Shim, SC ;

Yoon, KS ;

Chung, HT .

IMMUNOLOGY LETTERS, 2004, 95 (01) :91-95

[4] Apoptosis and interferons: Role of interferon-stimulated genes as mediators of apoptosis [J].

Chawla-Sarkar, M ;

Lindner, DJ ;

Liu, YF ;

Williams, B ;

Sen, GC ;

Silverman, RH ;

Borden, EC .

APOPTOSIS, 2003, 8 (03) :237-249

[5] Anti-IL-23 therapy inhibits multiple inflammatory pathways and ameliorates autoimmune encephalomyelitis [J].

Chen, Y ;

Langrish, CL ;

Mckenzie, B ;

Joyce-Shaikh, B ;

Stumhofer, JS ;

McClanahan, T ;

Blumenschein, W ;

Churakovsa, T ;

Low, J ;

Presta, L ;

Hunter, CA ;

Kastelein, RA ;

Cua, DJ .

JOURNAL OF CLINICAL INVESTIGATION, 2006, 116 (05) :1317-1326

[6]

Ferber IA, 1996, J IMMUNOL, V156, P5

[7] Cutting edge: T cell Ig mucin-3 reduces inflammatory heart disease by increasing CTLA-4 during innate immunity [J].

Frisancho-Kiss, Sylvia ;

Nyland, Jennifer F. ;

Davis, Sarah E. ;

Barrett, Masheka A. ;

Gatewood, Shannon J. L. ;

Njoku, Dolores B. ;

Cihakova, Daniela ;

Silbergeld, Ellen K. ;

Rose, Noel R. ;

Fairweather, DeLisa .

JOURNAL OF IMMUNOLOGY, 2006, 176 (11) :6411-6415

[8] Soluble form of T cell ig mucin 3 is an inhibitory molecule in T cell-mediated immune response [J].

Geng, H ;

Zhang, GM ;

Li, D ;

Zhang, H ;

Yuan, Y ;

Zhu, HG ;

Xiao, H ;

Han, LF ;

Feng, ZH .

JOURNAL OF IMMUNOLOGY, 2006, 176 (03) :1411-1420

[9] Congenic mapping of the diabetogenic locus Idd4 to a 5.2-cM region of chromosome 11 in NOD mice [J].

Grattan, M ;

Mi, QS ;

Meagher, C ;

Delovitch, TL .

DIABETES, 2002, 51 (01) :215-223

[10] Association of atopy and eczema with polymorphisms in T-cell immunoglobulin domain and mucin domain -: IL-2-inducible T-cell kinase gene cluster in chromosome 5q33 [J].

Graves, PE ;

Siroux, V ;

Guerra, S ;

Klimecki, WT ;

Martinez, FD .

JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2005, 116 (03) :650-656