Document Detail


Early signaling events that underlie fate decisions of naive CD4(+) T cells toward distinct T-helper cell subsets.
MedLine Citation:
PMID:  23405892     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
CD4(+) T-helper (Th) cells are a major cell population that play an important role in governing acquired immune responses to a variety of foreign antigens as well as inducing some types of autoimmune diseases. There are at least four distinct Th cell subsets (Th1, Th2, Th17, and inducible T-regulatory cells), each of which has specialized functions to control immune responses. Each of these cell types emerge from naive CD4(+) T cells after encounter with foreign antigens presented by dendritic cells (DCs). Each Th cell subset expresses a unique set of transcription factors and produces hallmark cytokines. Both T-cell receptor (TCR)-mediated stimulation and the cytokine environment created by activated CD4(+) T cells themselves, by 'partner' DCs, and/or other cell types during the course of differentiation, play an important role in the fate decisions toward distinct Th subsets. Here, we review how TCR-mediated signals in collaboration with the cytokine environment influence the fate decisions of naive CD4(+) T cells toward distinct Th subsets at the early stages of activation. We also discuss the roles of TCR-proximal signaling intermediates and of the Notch pathway in regulating the differentiation to distinct Th phenotypes.
Authors:
Hidehiro Yamane; William E Paul
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Intramural; Review    
Journal Detail:
Title:  Immunological reviews     Volume:  252     ISSN:  1600-065X     ISO Abbreviation:  Immunol. Rev.     Publication Date:  2013 Mar 
Date Detail:
Created Date:  2013-02-14     Completed Date:  2013-07-18     Revised Date:  2014-03-06    
Medline Journal Info:
Nlm Unique ID:  7702118     Medline TA:  Immunol Rev     Country:  England    
Other Details:
Languages:  eng     Pagination:  12-23     Citation Subset:  IM    
Copyright Information:
Published 2013. This article is a U.S. Government work and is in the public domain in the USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
CD4-Positive T-Lymphocytes / cytology,  immunology*
Cell Differentiation
Cytokines / biosynthesis,  immunology
Dendritic Cells / cytology,  immunology*
Gene Expression Regulation / immunology
Humans
Lymphocyte Activation
Mice
Receptors, Antigen, T-Cell / genetics,  immunology
Receptors, Notch / genetics,  immunology
Signal Transduction / immunology*
T-Lymphocyte Subsets / cytology,  immunology*
Transcription Factors / genetics,  immunology
Grant Support
ID/Acronym/Agency:
ZIA AI000493-26/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/Cytokines; 0/Receptors, Antigen, T-Cell; 0/Receptors, Notch; 0/Transcription Factors
Comments/Corrections
Erratum In:
Immunol Rev. 2013 Sep;255(1):275

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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