The latest study from the Jill Roberts Institute, "CX3CR1+ mononuclear phagocytes control immunity to intestinal fungi," was published on January 11 in Science. To read more, click here.  Dr. Gregory Sonnenberg wins inaugural award from the Society for Mucosal Immunology. To read more, click here.  The Kenneth Rainin Foundation awarded Dr. Iliyan Iliev and colleagues from Mount Sinai a $250,000 Synergy Award to examine the composition of the fungal community in babies born to mothers with inflammatory bowel disease. To read more, click here. Dr. Randy Longman received the Irma T. Hirschl Career Scientist Award and the New York Crohn’s Foundation Award.    

The Jill Roberts Institute for Research in Inflammatory Bowel Disease

You are here

Apoptosis in response to microbial infection induces autoreactive TH17 cells.

TitleApoptosis in response to microbial infection induces autoreactive TH17 cells.
Publication TypeJournal Article
Year of Publication2016
AuthorsCampisi, L, Barbet, G, Ding, Y, Esplugues, E, Flavell, RA, J Blander, M
JournalNat Immunol
Date Published2016 Sep

Microbial infections often precede the onset of autoimmunity. How infections trigger autoimmunity remains poorly understood. We investigated the possibility that infection might create conditions that allow the stimulatory presentation of self peptides themselves and that this might suffice to elicit autoreactive T cell responses that lead to autoimmunity. Self-reactive CD4(+) T cells are major drivers of autoimmune disease, but their activation is normally prevented through regulatory mechanisms that limit the immunostimulatory presentation of self antigens. Here we found that the apoptosis of infected host cells enabled the presentation of self antigens by major histocompatibility complex class II molecules in an inflammatory context. This was sufficient for the generation of an autoreactive TH17 subset of helper T cells, prominently associated with autoimmune disease. Once induced, the self-reactive TH17 cells promoted auto-inflammation and autoantibody generation. Our findings have implications for how infections precipitate autoimmunity.

Alternate JournalNat. Immunol.
PubMed ID27455420
PubMed Central IDPMC5079524
Grant ListP01 DK072201 / DK / NIDDK NIH HHS / United States
R01 AI073899 / AI / NIAID NIH HHS / United States
R01 AI095245 / AI / NIAID NIH HHS / United States
R21 AI080959 / AI / NIAID NIH HHS / United States
R56 AI073899 / AI / NIAID NIH HHS / United States