Here's the abstract (actually the first paragraph) from the Nature letter you pointed to:
Nature 415, 536 - 541 (2002)
Th1-specific cell surface protein Tim-3 regulates macrophage activation and severity of an autoimmune disease
LAURENT MONNEY*, CATHERINE A. SABATOS*, JASON L. GAGLIA*, AKEMI RYU*, HANSPETER WALDNER*, TATYANA CHERNOVA†, STEPHEN MANNING‡, EDWARD A. GREENFIELD*†, ANTHONY J. COYLE‡, RAYMOND A. SOBEL§, GORDON J. FREEMAN† & VIJAY K. KUCHROO*
* Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
† Department of Adult Oncology, Dana-Farber Cancer Institute and Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA
‡ Millennium Pharmaceuticals, 640 Memorial Drive, Cambridge, Massachusetts 02139, USA
§ VA Health Care System, Palo Alto and Department of Pathology, Stanford University School of Medicine, Stanford, California 95305, USA
Correspondence and requests for materials should be addressed to V.K.K. (e-mail: vkuchroo@rics.bwh.harvard.edu). The Tim-3 mRNA sequences have been deposited in GenBank under accession numbers AF450241–AF450243.
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)-, interleukin (IL)-2, tumour-necrosis factor (TNF)- 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.
Peter |
