| Transforming growth factor-beta: recent advances on its role in immune tolerance. | |
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MedLine Citation:
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PMID: 20941619 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Transforming growth factor (TGF-β1) is a pleiotropic cytokine, secreted by immune and nonhematopoietic cells. TGF-β is involved in many different critical processes, such as embryonal development, cellular maturation and differentiation, wound healing, and immune regulation. It maintains immune homeostasis by acting as a potent immune suppressor through inhibition of proliferation, differentiation, activation, and effector function of immune cells. Paradoxically, depending on the context, it displays proinflammatory properties by being a potent chemoattractant for neutrophils and promoting inflammation. In addition, it does not only induce differentiation into the anti-inflammatory Treg cells, but also into the proinflammatory Th17 and Th9 cells and inhibits Th22 differentiation. TGF-β has been demonstrated to be involved in multiple pathologies. In infections, it protects against collateral damages caused by the immune system, but it also promotes immune evasion and chronic infections. In autoimmune diseases, a TGF-β dysfunction leads to the loss of tolerance to self-antigens. In cancer, TGF-β is a potent inhibitor of cell proliferation and acts as a tumor suppressor at the beginning of tumorogenesis. However, once the cells become resistant to TGF-β, it mainly supports tumor growth and metastasis by promoting immune evasion and angiogenesis. In asthma, it is assumed to promote allergen tolerance, but plays a detrimental role in irreversible remodeling of the airways. Despite the high numbers of TGF-β-targeted pathways, it is a promising drug target for treatment of autoimmunity, cancer, fibrosis, if cell specificity can be achieved.This review summarizes the progresses that have been accomplished on the understanding of TGF-β's signaling in the immune homeostasis and its role in pathogenesis. |
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Authors:
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Pierre-Yves Mantel; Carsten B Schmidt-Weber |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Methods in molecular biology (Clifton, N.J.) Volume: 677 ISSN: 1940-6029 ISO Abbreviation: Methods Mol. Biol. Publication Date: 2011 |
Date Detail:
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Created Date: 2010-10-13 Completed Date: 2011-02-02 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9214969 Medline TA: Methods Mol Biol Country: United States |
Other Details:
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Languages: eng Pagination: 303-38 Citation Subset: IM |
Affiliation:
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Department of Immunology and Infectious Diseases, Harvard School of Public Health, Harvard University, Boston, MA, USA. pmantel@hsph.harvard.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Antigens, CD8
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pharmacology Arthritis, Rheumatoid / immunology Base Sequence Cells, Cultured Cytokines / physiology* Diabetes Mellitus, Type 1 / immunology Forkhead Transcription Factors / genetics* Gene Expression Regulation Humans Immune Tolerance / immunology* Interleukin-2 / pharmacology Interleukin-4 / pharmacology Malaria / immunology Molecular Sequence Data Multiple Sclerosis / immunology Promoter Regions, Genetic / genetics Signal Transduction / physiology Transcription Factors / genetics, metabolism* Transforming Growth Factor beta / physiology* Transforming Growth Factor beta1 / immunology Wound Healing / immunology |
| Chemical | |
Reg. No./Substance:
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0/Antigens, CD8; 0/Cytokines; 0/FOXP3 protein, human; 0/Forkhead Transcription Factors; 0/IL4 protein, human; 0/Interleukin-2; 0/Transcription Factors; 0/Transforming Growth Factor beta; 0/Transforming Growth Factor beta1; 207137-56-2/Interleukin-4 |
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