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      Transforming growth factor β: a master regulator of the gut microbiota and immune cell interactions

      review-article
      Author(s): 1 , 2 , 1 , 2 , *
      Publication date (Electronic):
      Journal: Clinical & Translational Immunology
      Publisher: Nature Publishing Group

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          Abstract

          The relationship between host organisms and their microbiota has co-evolved towards an inter-dependent network of mutualistic interactions. This interplay is particularly well studied in the gastrointestinal tract, where microbiota and host immune cells can modulate each other directly, as well as indirectly, through the production and release of chemical molecules and signals. In this review, we define the functional impact of transforming growth factor-beta (TGF-β) on this complex interplay, especially through its modulation of the activity of local regulatory T cells (Tregs), type 17 helper (Th17) cells, innate lymphoid cells (ILCs) and B cells.

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          Most cited references52

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          TGFbeta in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-producing T cells.

          Marc Veldhoen, Richard J Hocking, Christopher Atkins … (2006)
          We describe de novo generation of IL-17-producing T cells from naive CD4 T cells, induced in cocultures of naive CD4 T cells and naturally occurring CD4+ CD25+ T cells (Treg) in the presence of TLR3, TLR4, or TLR9 stimuli. Treg can be substituted by TGFbeta1, which, together with the proinflammatory cytokine IL-6, supports the differentiation of IL-17-producing T cells, a process that is amplified by IL-1beta and TNFalpha. We could not detect a role for IL-23 in the differentiation of IL-17-producing T cells but confirmed its importance for their survival and expansion. Transcription factors GATA-3 and T-bet, as well as its target Hlx, are absent in IL-17-producing T cells, and they do not express the negative regulator for TGFbeta signaling, Smad7. Our data indicate that, in the presence of IL-6, TGFbeta1 subverts Th1 and Th2 differentiation for the generation of IL-17-producing T cells.
          Article 0 comments Cited 874 times – based on 0 reviews     Review now
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            Targeted disruption of the mouse transforming growth factor-beta 1 gene results in multifocal inflammatory disease.

            M Shull, I Ormsby, A Kier … (1992)
            Transforming growth factor-beta 1 (TGF-beta 1) is a multifunctional growth factor that has profound regulatory effects on many developmental and physiological processes. Disruption of the TGF-beta 1 gene by homologous recombination in murine embryonic stem cells enables mice to be generated that carry the disrupted allele. Animals homozygous for the mutated TGF-beta 1 allele show no gross developmental abnormalities, but about 20 days after birth they succumb to a wasting syndrome accompanied by a multifocal, mixed inflammatory cell response and tissue necrosis, leading to organ failure and death. TGF-beta 1-deficient mice may be valuable models for human immune and inflammatory disorders, including autoimmune diseases, transplant rejection and graft versus host reactions.
            Article 0 comments Cited 483 times – based on 0 reviews     Review now
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              Transcriptional Programs Define Molecular Characteristics of Innate Lymphoid Cell Classes and Subsets

              Michelle Robinette, Anja Fuchs, Victor S. Cortez … (2015)
              The diversity of innate lymphoid cells (ILCs) is rapidly expanding. Three ILC classes have emerged, ILC1, ILC2, and ILC3, with ILC1 and ILC3 including several subsets. The classification of some subsets is unclear and it remains controversial whether NK cells and ILC1 are distinct cell types. To address these issues, we analyzed ILCs and NK cells gene expression within mouse small intestine, spleen, and liver, as part of the Immunological Genome Project. Results identify unique gene-expression patterns for some ILCs and overlapping patterns between ILC1 and NK cells, whereas few ILC subsets remain indistinguishable. A transcriptional program shared by small intestine ILCs and a core ILC signature is identified. Transcripts that suggest novel ILC functions and developmental paths are revealed and discussed.
              Article 0 comments Cited 289 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Clin Transl Immunology
                Journal ID (iso-abbrev): Clin Transl Immunology
                Title: Clinical & Translational Immunology
                Publisher: Nature Publishing Group
                ISSN (Electronic): 2050-0068
                Publication date Collection: April 2017
                Publication date (Electronic): 07 April 2017
                Publication date PMC-release: 1 April 2017
                Volume: 6
                Issue: 4
                Page: e136
                Affiliations
                [1 ]Department of Immunology, Virology and Inflammation, Cancer Research Center of Lyon UMR INSERM1052, CNRS 5286, Centre Léon Bérard Hospital, Université de Lyon, Equipe labellisée LIGUE , Lyon, France
                [2 ]TGF-β and Immuno-evasion Group, German Cancer Research Center (DKFZ) , Heidelberg, Germany
                Author notes
                [* ]Department of Immunology, Virology and Inflammation, Cancer Research Center of Lyon UMR INSERM1052, CNRS 5286, Centre Léon Bérard Hospital, Université de Lyon, Equipe labellisée LIGUE , 28 rue Laennec, F-69373 Lyon, France. E-mail: julien.marie@ 123456inserm.fr
                Article
                Publisher Item ID: cti20179
                DOI: 10.1038/cti.2017.9
                PMC ID: 5418590
                SO-VID: 00657be9-564b-496c-9dd6-48fb06388239
                Copyright © Copyright © 2017 The Author(s)
                License:

                This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/4.0/

                History
                Date received : 14 October 2016
                Date revision received : 20 February 2017
                Date accepted : 20 February 2017
                Categories
                Subject: Review

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