The Crohn’s disease polymorphism, ATG16L1 T300A, alters the gut microbiota and enhances the local Th1/Th17 response

Autor: Sydney Lavoie, Kara L Conway, Kara G Lassen, Humberto B Jijon, Hui Pan, Eunyoung Chun, Monia Michaud, Jessica K Lang, Carey Ann Gallini Comeau, Jonathan M Dreyfuss, Jonathan N Glickman, Hera Vlamakis, Ashwin Ananthakrishnan, Aleksander Kostic, Wendy S Garrett, Ramnik J Xavier

Publikováno v: eLife, Vol 8 (2019)

Inflammatory bowel disease (IBD) is driven by dysfunction between host genetics, the microbiota, and immune system. Knowledge gaps remain regarding how IBD genetic risk loci drive gut microbiota changes. The Crohn’s disease risk allele ATG16L1 T300

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The Crohn's disease polymorphism, ATG16L1 T300A, alters the gut microbiota and enhances the local Th1/Th17 response.

Autor: Lavoie S; Department of Immunology and Infectious Diseases, Harvard T. H. Chan School of Public Health, Boston, United States.; Department of Genetics and Complex Diseases, Harvard T. H. Chan School of Public Health, Boston, United States., Conway KL; Gastrointestinal Unit, Center for the Study of Inflammatory Bowel Disease, Massachusetts General Hospital, Boston, United States., Lassen KG; Broad Institute of Harvard and MIT, Cambridge, United States.; Center for Computational and Integrative Biology, Massachusetts General Hospital, Boston, United States., Jijon HB; Gastrointestinal Unit, Center for the Study of Inflammatory Bowel Disease, Massachusetts General Hospital, Boston, United States., Pan H; Joslin Diabetes Center, Boston, United States., Chun E; Department of Immunology and Infectious Diseases, Harvard T. H. Chan School of Public Health, Boston, United States.; Department of Genetics and Complex Diseases, Harvard T. H. Chan School of Public Health, Boston, United States., Michaud M; Department of Immunology and Infectious Diseases, Harvard T. H. Chan School of Public Health, Boston, United States.; Department of Genetics and Complex Diseases, Harvard T. H. Chan School of Public Health, Boston, United States., Lang JK; Department of Immunology and Infectious Diseases, Harvard T. H. Chan School of Public Health, Boston, United States.; Department of Genetics and Complex Diseases, Harvard T. H. Chan School of Public Health, Boston, United States., Gallini Comeau CA; Department of Immunology and Infectious Diseases, Harvard T. H. Chan School of Public Health, Boston, United States.; Department of Genetics and Complex Diseases, Harvard T. H. Chan School of Public Health, Boston, United States., Dreyfuss JM; Joslin Diabetes Center, Boston, United States., Glickman JN; Department of Pathology, Harvard Medical School, Boston, United States.; Beth Israel Deaconess Medical Center, Boston, United States., Vlamakis H; Broad Institute of Harvard and MIT, Cambridge, United States., Ananthakrishnan A; Gastrointestinal Unit, Center for the Study of Inflammatory Bowel Disease, Massachusetts General Hospital, Boston, United States., Kostic A; Joslin Diabetes Center, Boston, United States.; Department of Microbiology and Immunobiology, Harvard Medical School, Boston, United States., Garrett WS; Department of Immunology and Infectious Diseases, Harvard T. H. Chan School of Public Health, Boston, United States.; Department of Genetics and Complex Diseases, Harvard T. H. Chan School of Public Health, Boston, United States.; Broad Institute of Harvard and MIT, Cambridge, United States.; Department and Division of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, United States., Xavier RJ; Gastrointestinal Unit, Center for the Study of Inflammatory Bowel Disease, Massachusetts General Hospital, Boston, United States.; Broad Institute of Harvard and MIT, Cambridge, United States.

Publikováno v: ELife [Elife] 2019 Jan 22; Vol. 8. Date of Electronic Publication: 2019 Jan 22.