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
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
[11]   RECIPROCAL EXPRESSION OF INTERFERON-GAMMA OR INTERLEUKIN-4 DURING THE RESOLUTION OR PROGRESSION OF MURINE LEISHMANIASIS - EVIDENCE FOR EXPANSION OF DISTINCT HELPER T-CELL SUBSETS [J].
HEINZEL, FP ;
SADICK, MD ;
HOLADAY, BJ ;
COFFMAN, RL ;
LOCKSLEY, RM .
JOURNAL OF EXPERIMENTAL MEDICINE, 1989, 169 (01) :59-72
[12]   T cell Ig- and mucin-domain-containing molecule-3 (TIM-3) and TIM-1 molecules are differentially expressed on human Th1 and Th2 cells and in cerebrospinal fluid-derived mononuclear cells in multiple sclerosis [J].
Khademi, M ;
Illés, Z ;
Gielen, AW ;
Marta, M ;
Takazawa, N ;
Baecher-Allan, C ;
Brundin, L ;
Hannerz, J ;
Martin, C ;
Harris, RA ;
Hafler, DA ;
Kuchroo, VK ;
Olsson, T ;
Piehl, F ;
Wallström, E .
JOURNAL OF IMMUNOLOGY, 2004, 172 (11) :7169-7176
[13]   Dysregulated T cell expression of TIM3 in multiple sclerosis [J].
Koguchi, Ken ;
Anderson, David E. ;
Yang, Li ;
O'Connor, Kevin C. ;
Kuchroo, Vijay K. ;
Hafler, David A. .
JOURNAL OF EXPERIMENTAL MEDICINE, 2006, 203 (06) :1413-1418
[14]   Interleukin-17 family members and inflammation [J].
Kolls, JK ;
Lindén, A .
IMMUNITY, 2004, 21 (04) :467-476
[15]   Interferon-gamma confers resistance to experimental allergic encephalomyelitis [J].
Krakowski, M ;
Owens, T .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1996, 26 (07) :1641-1646
[16]   IL-23 drives a pathogenic T cell population that induces autoimmune inflammation [J].
Langrish, CL ;
Chen, Y ;
Blumenschein, WM ;
Mattson, J ;
Basham, B ;
Sedgwick, JD ;
McClanahan, T ;
Kastelein, RA ;
Cua, DJ .
JOURNAL OF EXPERIMENTAL MEDICINE, 2005, 201 (02) :233-240
[17]   Identification of Tapr (an airway hyperreactivity regulatory locus) and the linked Tim gene family [J].
McIntire, JJ ;
Umetsu, SE ;
Akbari, O ;
Potter, M ;
Kuchroo, VK ;
Barsh, GS ;
Freeman, GJ ;
Umetsu, DT ;
DeKruyff, RH .
NATURE IMMUNOLOGY, 2001, 2 (12) :1109-1116
[18]   Th1-specific cell surface protein Tim-3 regulates macrophage activation and severity of an autoimmune disease [J].
Monney, L ;
Sabatos, CA ;
Gaglia, JL ;
Ryu, A ;
Waldner, H ;
Chernova, T ;
Manning, S ;
Greenfield, EA ;
Coyle, AJ ;
Sobel, RA ;
Freeman, GJ ;
Kuchroo, VK .
NATURE, 2002, 415 (6871) :536-541
[19]   LYMPHOCYTE-RESPONSES AND CYTOKINES [J].
PAUL, WE ;
SEDER, RA .
CELL, 1994, 76 (02) :241-251
[20]   LYMPHOKINE PRODUCTION BY HUMAN T-CELLS IN DISEASE STATES [J].
ROMAGNANI, S .
ANNUAL REVIEW OF IMMUNOLOGY, 1994, 12 :227-257