Th1-specific cell surface protein Tim-3 regulates macrophage activation and severity of an autoimmune disease.

Authors: Monney, L  Sabatos, CA  Gaglia, JL  Ryu, A  Waldner, H  Chernova, T  Manning, S  Greenfield, EA  Coyle, AJ  Sobel, RA  Freeman, GJ  Kuchroo, VK 
Citation: Monney L, etal., Nature. 2002 Jan 31;415(6871):536-41.
Pubmed: (View Article at PubMed) PMID:11823861
DOI: Full-text: DOI:10.1038/415536a

Activation of naive CD4(+) T-helper cells results in the development of at least two distinct effector populations, Th1 and Th2 cells. Th1 cells produce cytokines (interferon (IFN)-gamma, interleukin (IL)-2, tumour-necrosis factor (TNF)-alpha and lymphotoxin) that are commonly associated with cell-mediated immune responses against intracellular pathogens, delayed-type hypersensitivity reactions, and induction of organ-specific autoimmune diseases. Th2 cells produce cytokines (IL-4, IL-10 and IL-13) that are crucial for control of extracellular helminthic infections and promote atopic and allergic diseases. Although much is known about the functions of these two subsets of T-helper cells, there are few known surface molecules that distinguish between them. We report here the identification and characterization of a transmembrane protein, Tim-3, which contains an immunoglobulin and a mucin-like domain and is expressed on differentiated Th1 cells. In vivo administration of antibody to Tim-3 enhances the clinical and pathological severity of experimental autoimmune encephalomyelitis (EAE), a Th1-dependent autoimmune disease, and increases the number and activation level of macrophages. Tim-3 may have an important role in the induction of autoimmune diseases by regulating macrophage activation and/or function.

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CRRD ID: 9686086
Created: 2015-01-30
Species: All species
Last Modified: 2015-01-30
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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.