Journal
EUROPEAN JOURNAL OF IMMUNOLOGY
Volume 40, Issue 3, Pages 859-866Publisher
WILEY
DOI: 10.1002/eji.200939842
Keywords
Autoimmunity; T cells; Transcription factors
Categories
Funding
- National Multiple Sclerosis Society MS [RG2571D9, FG1478A1]
- National Institutes of Health [NSO45937, NS35685, NS30843, A144880, AI139671, NS38037, NS054096, GM20927, CA112663]
- Medical Research Council [G0802068, G0600698B] Funding Source: researchfish
- MRC [G0802068] Funding Source: UKRI
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T-cell immunoglobulin, mucin domain-3 (Tim-3) is a membrane protein expressed at late stages of IFN-gamma secreting CD4(+) Th1 cell differentiation and constitutively on DC. Ligation of Tim-3 on Th1 cells terminates Th1 immune responses. In addition, Tim-3 plays a role in tolerance induction, although the mechanism by which this is accomplished has yet to be elucidated. While it is clear that Tim-3 plays an important role in the immune system, little is known regarding the molecular pathways that regulate Tim-3 expression. In the current study, we examine the role of Th1-associated transcription factors in regulating Tim-3 expression. Our experiments reveal that Tim-3 expression is regulated by the Th1-specific transcription factor T-bet. This introduces a novel paradigm into the generation of a Th1 response, whereby a transcription factor responsible for effector Th1 cell differentiation also increases the expression of a specific counter-regulatory molecule to ensure appropriate termination of pro-inflammatory Th1 immune responses.
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