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  • 1
    Publication Date: 2012-08-28
    Description: The mammalian gastrointestinal tract contains a large and diverse population of commensal bacteria and is also one of the primary sites of exposure to pathogens. How the immune system perceives commensals in the context of mucosal infection is unclear. Here, we show that during a gastrointestinal infection, tolerance to commensals is lost, and microbiota-specific T cells are activated and differentiate to inflammatory effector cells. Furthermore, these T cells go on to form memory cells that are phenotypically and functionally consistent with pathogen-specific T cells. Our results suggest that during a gastrointestinal infection, the immune response to commensals parallels the immune response against pathogenic microbes and that adaptive responses against commensals are an integral component of mucosal immunity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3784339/" 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/PMC3784339/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hand, Timothy W -- Dos Santos, Liliane M -- Bouladoux, Nicolas -- Molloy, Michael J -- Pagan, Antonio J -- Pepper, Marion -- Maynard, Craig L -- Elson, Charles O 3rd -- Belkaid, Yasmine -- DK071176/DK/NIDDK NIH HHS/ -- DK64400/DK/NIDDK NIH HHS/ -- R24 DK064400/DK/NIDDK NIH HHS/ -- T32 AI007051/AI/NIAID NIH HHS/ -- Z99 AI999999/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2012 Sep 21;337(6101):1553-6. Epub 2012 Aug 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mucosal Immunology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22923434" target="_blank"〉PubMed〈/a〉
    Keywords: Acute Disease ; Animals ; Bacteria/*immunology ; Bacterial Translocation ; CD4-Positive T-Lymphocytes/*immunology ; Flagellin/immunology ; Gastrointestinal Tract/*immunology/microbiology/parasitology ; *Immunity, Mucosal ; Immunologic Memory ; Intestinal Diseases, Parasitic/*immunology/parasitology ; Intestinal Mucosa/microbiology/parasitology ; Lymphocyte Activation ; Metagenome/*immunology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Th1 Cells/immunology ; Time Factors ; Toxoplasma/immunology/physiology ; Toxoplasmosis, Animal/*immunology/parasitology
    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: 2016-01-30
    Description: Infection elicits CD4(+) memory T lymphocytes that participate in protective immunity. Although memory cells are the progeny of naive T cells, it is unclear that all naive cells from a polyclonal repertoire have memory cell potential. Using a single-cell adoptive transfer and spleen biopsy method, we found that in mice, essentially all microbe-specific naive cells produced memory cells during infection. Different clonal memory cell populations had different B cell or macrophage helper compositions that matched effector cell populations generated much earlier in the response. Thus, each microbe-specific naive CD4(+) T cell produces a distinctive ratio of effector cell types early in the immune response that is maintained as some cells in the clonal population become memory cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4776317/" 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/PMC4776317/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tubo, Noah J -- Fife, Brian T -- Pagan, Antonio J -- Kotov, Dmitri I -- Goldberg, Michael F -- Jenkins, Marc K -- F32 AI107995/AI/NIAID NIH HHS/ -- R01 AI039614/AI/NIAID NIH HHS/ -- R01 AI106791/AI/NIAID NIH HHS/ -- T32 HL007062/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 29;351(6272):511-4. doi: 10.1126/science.aad0483.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immune Mediated Disease Therapy Group, Genzyme, a Sanofi Company, Framingham, MA 01701, USA. ; Department of Medicine, Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455, USA. ; Department of Medicine, MRC Laboratory of Molecular Biology, Cambridge, UK. ; Department of Microbiology and Immunology, Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455, USA. ; Department of Microbiology and Immunology, Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455, USA. jenki002@umn.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26823430" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; B-Lymphocytes/immunology ; Bacterial Toxins/immunology ; CD4-Positive T-Lymphocytes/*immunology/*microbiology ; Clone Cells/immunology ; Heat-Shock Proteins/immunology ; Hemolysin Proteins/immunology ; *Immunologic Memory ; Listeria monocytogenes/*immunology ; Listeriosis/*immunology ; Mice ; Mice, Inbred C57BL ; Receptors, CXCR5/genetics/immunology ; Single-Cell Analysis
    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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