MHC variation sculpts individualized microbial communities that control susceptibility to enteric infection
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. Jensen,
Ryan M. O’Connell and
June L. Round ()
Additional contact information
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
Joseph F. Petrosino: 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
Nature Communications, 2015, vol. 6, issue 1, 1-13
Abstract:
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.
Date: 2015
References: Add references at CitEc
Citations: View citations in EconPapers (1)
Downloads: (external link)
https://www.nature.com/articles/ncomms9642 Abstract (text/html)
Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.
Export reference: BibTeX
RIS (EndNote, ProCite, RefMan)
HTML/Text
Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms9642
Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/
DOI: 10.1038/ncomms9642
Access Statistics for this article
Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie
More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().