Source:http://linkedlifedata.com/resource/pubmed/id/11823861
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
6871
|
| pubmed:dateCreated |
2002-2-1
|
| pubmed:databankReference | |
| pubmed:abstractText |
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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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jan
|
| pubmed:issn |
0028-0836
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| pubmed:author |
pubmed-author:ChernovaTatyanaT,
pubmed-author:CoyleAnthony JAJ,
pubmed-author:FreemanGordon JGJ,
pubmed-author:GagliaJason LJL,
pubmed-author:GreenfieldEdward AEA,
pubmed-author:KuchrooVijay KVK,
pubmed-author:ManningStephenS,
pubmed-author:MonneyLaurentL,
pubmed-author:RyuAkemiA,
pubmed-author:SabatosCatherine ACA,
pubmed-author:SobelRaymond ARA,
pubmed-author:WaldnerHanspeterH
|
| pubmed:issnType |
Print
|
| pubmed:day |
31
|
| pubmed:volume |
415
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
536-41
|
| pubmed:dateRevised |
2006-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:11823861-Amino Acid Sequence,
pubmed-meshheading:11823861-Animals,
pubmed-meshheading:11823861-Antigens, CD11,
pubmed-meshheading:11823861-Cloning, Molecular,
pubmed-meshheading:11823861-Encephalomyelitis, Autoimmune, Experimental,
pubmed-meshheading:11823861-Female,
pubmed-meshheading:11823861-Gene Expression Profiling,
pubmed-meshheading:11823861-Humans,
pubmed-meshheading:11823861-Leukopoiesis,
pubmed-meshheading:11823861-Macrophage Activation,
pubmed-meshheading:11823861-Membrane Proteins,
pubmed-meshheading:11823861-Mice,
pubmed-meshheading:11823861-Mice, Inbred C57BL,
pubmed-meshheading:11823861-Mice, Transgenic,
pubmed-meshheading:11823861-Molecular Sequence Data,
pubmed-meshheading:11823861-Rats,
pubmed-meshheading:11823861-Rats, Inbred Lew,
pubmed-meshheading:11823861-Rats, Sprague-Dawley,
pubmed-meshheading:11823861-Receptors, Virus,
pubmed-meshheading:11823861-Th1 Cells
|
| pubmed:year |
2002
|
| pubmed:articleTitle |
Th1-specific cell surface protein Tim-3 regulates macrophage activation and severity of an autoimmune disease.
|
| pubmed:affiliation |
Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|