+1 Recommend
2 collections
      • Record: found
      • Abstract: found
      • Article: found

      Commensal microbiota drive proliferation of conventional and Foxp3 + Regulatory CD4 + T cells in mesenteric lymph nodes and Peyer's patches

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.


          Compelling evidence demonstrates that intestinal commensal microbiota modulate conventional and regulatory T cell (Treg) responses that are required for effective host defence against pathogens and avoidance of autoimmunity and other immunopathologic conditions. Here, we investigated the contribution of the commensal microbiota and Toll-like receptor (TLR) signaling to homeostasis of Foxp3 conventional CD4 + T cells and Foxp3 + Tregs. Upon long-term antibiotics treatment, we observed a significant reduction of conventional CD4 + T cell proliferation in a systemic manner, whereas Foxp3 + Treg proliferation was locally impaired in gut-draining mesenteric lymph nodes and Peyer's patches. The proliferative response to microbial components was not mediated by TLRs as MyD88- and various TLR-deficient mice displayed normal or even increased conventional T cell and Foxp3 + Treg proliferation. Thus, commensal microbiota-derived stimuli support cycling of both conventional CD4 + T cells and Foxp3 + Tregs with TLR-mediated recognition of bacterial components not being the major mechanism controlling microbiota-driven T cell homeostasis.

          Related collections

          Most cited references 48

          • Record: found
          • Abstract: found
          • Article: not found

          Recognition of commensal microflora by toll-like receptors is required for intestinal homeostasis.

          Toll-like receptors (TLRs) play a crucial role in host defense against microbial infection. The microbial ligands recognized by TLRs are not unique to pathogens, however, and are produced by both pathogenic and commensal microorganisms. It is thought that an inflammatory response to commensal bacteria is avoided due to sequestration of microflora by surface epithelia. Here, we show that commensal bacteria are recognized by TLRs under normal steady-state conditions, and this interaction plays a crucial role in the maintenance of intestinal epithelial homeostasis. Furthermore, we find that activation of TLRs by commensal microflora is critical for the protection against gut injury and associated mortality. These findings reveal a novel function of TLRs-control of intestinal epithelial homeostasis and protection from injury-and provide a new perspective on the evolution of host-microbial interactions.
            • Record: found
            • Abstract: found
            • Article: not found

            Targeted disruption of the MyD88 gene results in loss of IL-1- and IL-18-mediated function.

            MyD88, originally isolated as a myeloid differentiation primary response gene, is shown to act as an adaptor in interleukin-1 (IL-1) signaling by interacting with both the IL-1 receptor complex and IL-1 receptor-associated kinase (IRAK). Mice generated by gene targeting to lack MyD88 have defects in T cell proliferation as well as induction of acute phase proteins and cytokines in response to IL-1. Increases in interferon-gamma production and natural killer cell activity in response to IL-18 are abrogated. In vivo Th1 response is also impaired. Furthermore, IL-18-induced activation of NF-kappaB and c-Jun N-terminal kinase (JNK) is blocked in MyD88-/- Th1-developing cells. Taken together, these results demonstrate that MyD88 is a critical component in the signaling cascade that is mediated by IL-1 receptor as well as IL-18 receptor.
              • Record: found
              • Abstract: not found
              • Article: not found

              Interactions between commensal intestinal bacteria and the immune system.


                Author and article information

                European Journal of Microbiology and Immunology
                Akadémiai Kiadó, co-published with Springer Science+Business Media B.V., Formerly Kluwer Academic Publishers B.V.
                1 March 2013
                : 3
                : 1
                : 1-10
                [ 1 ] Experimental Immunology, Helmholtz Centre for Infection Research, 38124, Braunschweig, Germany
                [ 2 ] Institute for Microbiology and Hygiene, Charité University Medicine Berlin, Campus Benjamin Franklin, 12200, Berlin, Germany
                [ 3 ] Department of Pathology, Charité University Medicine Berlin, Campus Benjamin Franklin, 12200, Berlin, Germany
                [ 4 ] Division of Innate Immune Regulation, International Research and Development Center for Mucosal Vaccine, The Institute of Medical Science, University of Tokyo, 108-8639, Tokyo, Japan
                [ 5 ] Laboratory of Host Defense, WPI Immunology Frontier Research Center, Osaka, University, 3-1 Yamada-oka, Suita, Osaka, 565-0871, Japan
                [ 6 ] Experimental Rheumatology, Charité University Medicine Berlin, Campus Mitte, 10117, Berlin, Germany
                [ 7 ] Experimental Immunology, Helmholtz Centre for Infection Research, Inhoffenstr. 7, D-38124, Braunschweig, Germany
                [ 8 ] Lymphoid Tissue Development Unit, Institut Pasteur, Paris, France
                Author notes
                [* ] +49-531-6181-3310, +49-531-6181-3399, jochen.huehn@ 123456helmholtz-hzi.de


                Comment on this article