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Development and Survival of Th17 Cells within the Intestines: The Influence of Microbiome- and Diet-Derived Signals

Joseph H. Chewning and Casey T. Weaver
J Immunol November 15, 2014, 193 (10) 4769-4777; DOI: https://doi.org/10.4049/jimmunol.1401835
Joseph H. Chewning
*Department of Pediatrics, Pediatric Blood and Marrow Transplantation Program, University of Alabama at Birmingham, Birmingham, AL 35294; and
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Casey T. Weaver
†Department of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294
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Abstract

Th17 cells have emerged as important mediators of host defense and homeostasis at barrier sites, particularly the intestines, where the greatest number and diversity of the microbiota reside. A critical balance exists between protection of the host from its own microbiota and pathogens and the development of immune-mediated disease. Breaches of local innate immune defenses provide critical stimuli for the induction of Th17 cell development, and additional cues within these tissues promote Th17 cell survival and/or plasticity. Normally, this results in eradication of the microbial threat and restitution of homeostasis. When dysregulated, however, Th17 cells can cause a range of immune-mediated diseases, whether directed against Ags derived from the microbiota, such as in inflammatory bowel disease, or against self-Ags in a range of autoimmune diseases. This review highlights recent discoveries that provide new insights into ways in which environmental signals impact Th17 cell development and function in the intestines.

Footnotes

  • Abbreviations used in this article:

    Ahr
    aryl hydrocarbon receptor
    CD
    Crohn’s disease
    DC
    dendritic cell
    DSS
    dextran sulfate sodium
    EAE
    experimental autoimmune encephalitis
    ENTPDase
    ectonucleoside triphosphate diphosphohydrolase
    GI
    gastrointestinal
    HIF-1
    hypoxia-inducible factor 1
    IBD
    inflammatory bowel disease
    IEC
    intestinal epithelial cell
    LP
    lamina propria
    MLN
    mesenteric lymph node
    PRR
    pattern recognition receptor
    pTreg
    peripheral regulatory T cell
    SCFA
    short-chain fatty acid
    SFB
    segmented filamentous bacteria
    SILP
    small intestine LP
    Treg
    regulatory T cell
    UC
    ulcerative colitis.

  • Received August 11, 2014.
  • Accepted August 25, 2014.
  • Copyright © 2014 by The American Association of Immunologists, Inc.
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The Journal of Immunology: 193 (10)
The Journal of Immunology
Vol. 193, Issue 10
15 Nov 2014
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Development and Survival of Th17 Cells within the Intestines: The Influence of Microbiome- and Diet-Derived Signals
Joseph H. Chewning, Casey T. Weaver
The Journal of Immunology November 15, 2014, 193 (10) 4769-4777; DOI: 10.4049/jimmunol.1401835

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Development and Survival of Th17 Cells within the Intestines: The Influence of Microbiome- and Diet-Derived Signals
Joseph H. Chewning, Casey T. Weaver
The Journal of Immunology November 15, 2014, 193 (10) 4769-4777; DOI: 10.4049/jimmunol.1401835
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    • Abstract
    • IL-23 signaling is critical for both Th17 cell survival and plasticity
    • Role of IL-1β in stabilizing the Th17 phenotype
    • Importance of aryl hydrocarbon receptor ligands and ATP produced by microbiota in Th17 development and survival
    • Other environmental and dietary effects on Th17 development
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