Microbiota therapy acts via a regulatory T cell MyD88/RORγt pathway to suppress food allergy | Zendy

Azza Abdel-Gadir | Zendy; Emmanuel StephenVictor | Zendy; Georg K. Gerber | Zendy; Magali Noval Rivas | Zendy; Sen Wang | Zendy; Hani Harb | Zendy; Leighanne Wang | Zendy; Ning Li | Zendy; Elena Crestani | Zendy; Sara Spielman | Zendy; W. Evan Secor | Zendy; Heather Biehl | Zendy; Nicholas DiBenedetto | Zendy; Xiaoxi Dong | Zendy; Dale T. Umetsu | Zendy; Lynn Bry | Zendy; Rima Rachid | Zendy; Talal A. Chatila | Zendy

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Microbiota therapy acts via a regulatory T cell MyD88/RORγt pathway to suppress food allergy

Author(s) -

Azza Abdel-Gadir,

Emmanuel StephenVictor,

Georg K. Gerber,

Magali Noval Rivas,

Sen Wang,

Hani Harb,

Leighanne Wang,

Ning Li,

Elena Crestani,

Sara Spielman,

W. Evan Secor,

Heather Biehl,

Nicholas DiBenedetto,

Xiaoxi Dong,

Dale T. Umetsu,

Lynn Bry,

Rima Rachid,

Talal A. Chatila

Publication year - 2019

Publication title -

nature medicine

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 19.536

H-Index - 547

eISSN - 1546-170X

pISSN - 1078-8956

DOI - 10.1038/s41591-019-0461-z

Subject(s) - dysbiosis , rar related orphan receptor gamma , immunology , biology , foxp3 , regulatory t cell , allergy , immune system , gut flora , transcription factor , food allergy , medicine , t cell , microbiology and biotechnology , il 2 receptor , gene , genetics

The role of dysbiosis in food allergy (FA) remains unclear. We found that dysbiotic fecal microbiota in FA infants evolved compositionally over time and failed to protect against FA in mice. Infants and mice with FA had decreased IgA and increased IgE binding to fecal bacteria, indicative of a broader breakdown of oral tolerance than hitherto appreciated. Therapy with Clostridiales species impacted by dysbiosis, either as a consortium or as monotherapy with Subdoligranulum variabile, suppressed FA in mice as did a separate immunomodulatory Bacteroidales consortium. Bacteriotherapy induced expression by regulatory T (Treg) cells of the transcription factor ROR-γt in a MyD88-dependent manner, which was deficient in FA infants and mice and ineffectively induced by their microbiota. Deletion of Myd88 or Rorc in Treg cells abrogated protection by bacteriotherapy. Thus, commensals activate a MyD88/ROR-γt pathway in nascent Treg cells to protect against FA, while dysbiosis impairs this regulatory response to promote disease.

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