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MHC variation sculpts individualized microbial communities that control susceptibility to enteric infection

Author

Listed:
  • Jason L. Kubinak

    (University of Utah School of Medicine)

  • W. Zac Stephens

    (University of Utah School of Medicine)

  • Ray Soto

    (University of Utah School of Medicine)

  • Charisse Petersen

    (University of Utah School of Medicine)

  • Tyson Chiaro

    (University of Utah School of Medicine)

  • Lasha Gogokhia

    (University of Utah School of Medicine)

  • Rickesha Bell

    (University of Utah School of Medicine)

  • Nadim J. Ajami

    (Baylor College of Medicine
    Alkek Center for Metagenomics and Microbiome Research, Baylor College of Medicine)

  • Joseph F. Petrosino

    (Baylor College of Medicine
    Alkek Center for Metagenomics and Microbiome Research, Baylor College of Medicine)

  • Linda Morrison

    (University of Utah)

  • Wayne K. Potts

    (University of Utah)

  • Peter E. Jensen

    (University of Utah School of Medicine)

  • Ryan M. O’Connell

    (University of Utah School of Medicine)

  • June L. Round

    (University of Utah School of Medicine)

Abstract

The presentation of protein antigens on the cell surface by major histocompatibility complex (MHC) molecules coordinates vertebrate adaptive immune responses, thereby mediating susceptibility to a variety of autoimmune and infectious diseases. The composition of symbiotic microbial communities (the microbiota) is influenced by host immunity and can have a profound impact on host physiology. Here we use an MHC congenic mouse model to test the hypothesis that genetic variation at MHC genes among individuals mediates susceptibility to disease by controlling microbiota composition. We find that MHC genotype significantly influences antibody responses against commensals in the gut, and that these responses are correlated with the establishment of unique microbial communities. Transplantation experiments in germfree mice indicate that MHC-mediated differences in microbiota composition are sufficient to explain susceptibility to enteric infection. Our findings indicate that MHC polymorphisms contribute to defining an individual’s unique microbial fingerprint that influences health.

Suggested Citation

  • Jason L. Kubinak & W. Zac Stephens & Ray Soto & Charisse Petersen & Tyson Chiaro & Lasha Gogokhia & Rickesha Bell & Nadim J. Ajami & Joseph F. Petrosino & Linda Morrison & Wayne K. Potts & Peter E. Je, 2015. "MHC variation sculpts individualized microbial communities that control susceptibility to enteric infection," Nature Communications, Nature, vol. 6(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms9642
    DOI: 10.1038/ncomms9642
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    Cited by:

    1. Allison F Christiaansen & Megan E Schmidt & Stacey M Hartwig & Steven M Varga, 2017. "Host genetics play a critical role in controlling CD8 T cell function and lethal immunopathology during chronic viral infection," PLOS Pathogens, Public Library of Science, vol. 13(7), pages 1-19, July.

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