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  • Germ-Free Life  (2)
  • American Association for the Advancement of Science (AAAS)  (2)
  • 1
    Publication Date: 2011-01-06
    Description: CD4(+) T regulatory cells (T(regs)), which express the Foxp3 transcription factor, play a critical role in the maintenance of immune homeostasis. Here, we show that in mice, T(regs) were most abundant in the colonic mucosa. The spore-forming component of indigenous intestinal microbiota, particularly clusters IV and XIVa of the genus Clostridium, promoted T(reg) cell accumulation. Colonization of mice by a defined mix of Clostridium strains provided an environment rich in transforming growth factor-beta and affected Foxp3(+) T(reg) number and function in the colon. Oral inoculation of Clostridium during the early life of conventionally reared mice resulted in resistance to colitis and systemic immunoglobulin E responses in adult mice, suggesting a new therapeutic approach to autoimmunity and allergy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3969237/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3969237/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Atarashi, Koji -- Tanoue, Takeshi -- Shima, Tatsuichiro -- Imaoka, Akemi -- Kuwahara, Tomomi -- Momose, Yoshika -- Cheng, Genhong -- Yamasaki, Sho -- Saito, Takashi -- Ohba, Yusuke -- Taniguchi, Tadatsugu -- Takeda, Kiyoshi -- Hori, Shohei -- Ivanov, Ivaylo I -- Umesaki, Yoshinori -- Itoh, Kikuji -- Honda, Kenya -- R00 DK085329/DK/NIDDK NIH HHS/ -- R01 AI052359/AI/NIAID NIH HHS/ -- R01 AI056154/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2011 Jan 21;331(6015):337-41. doi: 10.1126/science.1198469. Epub 2010 Dec 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Graduate School of Medicine, University of Tokyo, Tokyo 113-0033, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21205640" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/pharmacology ; Cecum/microbiology ; Cells, Cultured ; Clostridium/growth & development/*immunology ; Colitis/immunology/pathology/prevention & control ; Colon/*immunology/metabolism/*microbiology ; Feces/microbiology ; Forkhead Transcription Factors/metabolism ; Germ-Free Life ; Immunity, Innate ; Immunoglobulin E/biosynthesis ; Interleukin-10/immunology/metabolism ; Intestinal Mucosa/*immunology/metabolism ; Intestine, Small/immunology ; Metagenome ; Mice ; Mice, Inbred A ; Mice, Inbred BALB C ; Receptors, Pattern Recognition/physiology ; Specific Pathogen-Free Organisms ; T-Lymphocytes, Helper-Inducer/immunology ; T-Lymphocytes, Regulatory/*immunology/metabolism ; Transforming Growth Factor beta/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2015-07-15
    Description: Changes to the symbiotic microbiota early in life, or the absence of it, can lead to exacerbated type 2 immunity and allergic inflammations. Although it is unclear how the microbiota regulates type 2 immunity, it is a strong inducer of proinflammatory T helper 17 (T(H)17) cells and regulatory T cells (T(regs)) in the intestine. Here, we report that microbiota-induced T(regs) express the nuclear hormone receptor RORgammat and differentiate along a pathway that also leads to T(H)17 cells. In the absence of RORgammat(+) T(regs), T(H)2-driven defense against helminths is more efficient, whereas T(H)2-associated pathology is exacerbated. Thus, the microbiota regulates type 2 responses through the induction of type 3 RORgammat(+) T(regs) and T(H)17 cells and acts as a key factor in balancing immune responses at mucosal surfaces.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ohnmacht, Caspar -- Park, Joo-Hong -- Cording, Sascha -- Wing, James B -- Atarashi, Koji -- Obata, Yuuki -- Gaboriau-Routhiau, Valerie -- Marques, Rute -- Dulauroy, Sophie -- Fedoseeva, Maria -- Busslinger, Meinrad -- Cerf-Bensussan, Nadine -- Boneca, Ivo G -- Voehringer, David -- Hase, Koji -- Honda, Kenya -- Sakaguchi, Shimon -- Eberl, Gerard -- New York, N.Y. -- Science. 2015 Aug 28;349(6251):989-93. doi: 10.1126/science.aac4263. Epub 2015 Jul 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut Pasteur, Microenvironment and Immunity Unit, 75724 Paris, France. ; Laboratory of Experimental Immunology, Immunology Frontier Research Center, Osaka University, Suita 565-0871, Japan. ; RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Yokohama, Kanagawa 230-0045, Japan. PRESTO, Japan Science and Technology Agency, Saitama 332-0012, Japan. ; The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan. ; INSERM, U1163, Laboratory of Intestinal Immunity, Paris, France. Universite Paris Descartes-Sorbonne Paris Cite and Institut Imagine, Paris, France. INRA Micalis UMR1319, Jouy-en-Josas, France. ; Center of Allergy and Environment (ZAUM), Technische Universitat and Helmholtz Zentrum Munchen, Munich, Germany. ; Research Institute of Molecular Pathology, Vienna Biocenter, 1030 Vienna, Austria. ; INSERM, U1163, Laboratory of Intestinal Immunity, Paris, France. Universite Paris Descartes-Sorbonne Paris Cite and Institut Imagine, Paris, France. ; Institut Pasteur, Biology and Genetics of Bacterial Cell Wall, 75724 Paris, France. INSERM, Groupe Avenir, 75015 Paris, France. ; Department of Infection Biology at the Institute of Clinical Microbiology, Immunology and Hygiene, University Clinic Erlangen and Friedrich-Alexander University Erlangen-Nuremberg, 91054 Erlangen, Germany. ; RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Yokohama, Kanagawa 230-0045, Japan. CREST, Japan Science and Technology Agency, 4-1-8 Honcho Kawaguchi, Saitama 332-0012, Japan. ; Laboratory of Experimental Immunology, Immunology Frontier Research Center, Osaka University, Suita 565-0871, Japan. Department of Experimental Pathology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8507, Japan. ; Institut Pasteur, Microenvironment and Immunity Unit, 75724 Paris, France. gerard.eberl@pasteur.fr.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26160380" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Colitis, Ulcerative/immunology ; Colon/immunology/microbiology ; Germ-Free Life ; Homeostasis ; *Immunity, Mucosal ; Intestinal Mucosa/*immunology/*microbiology ; Intestine, Small/immunology/microbiology ; Intestines/immunology/*microbiology ; Mice ; Microbiota/*immunology ; Models, Immunological ; Nematospiroides dubius ; Nuclear Receptor Subfamily 1, Group F, Member 3/*metabolism ; Specific Pathogen-Free Organisms ; Strongylida Infections/immunology ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes, Regulatory/*immunology/metabolism ; Th17 Cells/immunology ; Th2 Cells/immunology ; Vitamin A/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
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