Document Detail


TGF-β Function in Immune Suppression.
MedLine Citation:
PMID:  20680806     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
Transforming growth factor-β (TGF-β) has been shown to play an essential role in establishing immunological tolerance, yet recent studies have revealed the pro-inflammatory roles of TGF-β in inflammatory responses. TGF-β induces Foxp3-positive regulatory T cells (iTregs), while in the presence of IL-6, it induces pathogenic IL-17 producing Th17 cells. TGF-β inhibits the proliferation of T cells as well as cytokine production via Foxp3-dependent and independent mechanisms. On the one hand, little is known about molecular mechanisms involved in immune suppression via TGF-β; however, recent studies suggest that Smad2 as well as Smad3 play essential roles in Foxp3 induction and cytokine suppression, whereas Th17 differentiation is promoted via the Smad-independent pathway. Mutual suppression of signaling between TGF-β and inflammatory cytokines has been shown to be necessary for the balance of immunity and tolerance.
Authors:
Akihiko Yoshimura; Go Muto
Related Documents :
22325826 - Daf/cd55 and protectin/cd59 modulate adaptive immunity and disease outcome in experimen...
19082496 - The platelet-derived growth factor receptor as a target for vascular endothelial growth...
16125646 - Leukemia inhibitory factor triggers activation of signal transducer and activator of tr...
8858926 - Ethanol inhibits basic fibroblast growth factor-mediated proliferation of c6 astrocytom...
22479266 - Fas ligand has a greater impact than tnf-α on apoptosis and inflammation in ischemic a...
16920916 - Humoral immune response to flagellin requires t cells and activation of innate immunity.
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Current topics in microbiology and immunology     Volume:  350     ISSN:  0070-217X     ISO Abbreviation:  Curr. Top. Microbiol. Immunol.     Publication Date:  2011  
Date Detail:
Created Date:  2011-04-11     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0110513     Medline TA:  Curr Top Microbiol Immunol     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  127-47     Citation Subset:  IM    
Affiliation:
Department of Microbiology and Immunology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan, yoshimura@a6.keio.jp.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

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


Previous Document:  Immunoregulatory roles for fc receptor-like molecules.
Next Document:  Fc?Rs in Health and Disease.