A model of TH17-associated ileal hyperplasia that requires both IL-17A and IFNγ to generate self-tolerance and prevent colitis View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2018-07

AUTHORS

Jonathan C. Jeschke, Christopher G. Mayne, Jennifer Ziegelbauer, Christopher L. DeCiantis, Selina Singh, Suresh N. Kumar, Mariko Suchi, Yoichiro Iwakura, William R. Drobyski, Nita H Salzman, Calvin B. Williams

ABSTRACT

Homeostasis in the ileum, which is commonly disrupted in patients with Crohn's disease, involves ongoing immune responses. To study how homeostatic processes of the ileum impact CD4+T cell responses, we used TCR transgenic tools to breed mice that spontaneously produced CD4+T cells reactive to an antigen expressed in the ileum. At an early age, the ilea of these mice exhibit crypt hyperplasia and accumulate increased numbers of TH17 cells bearing non-transgenic clonotypes. Half of these mice subsequently developed colitis linked to broad mucosal infiltration by TH17 and TH1 cells expressing non-transgenic clonotypes, chronic wasting disease and loss of ileal crypt hyperplasia. By contrast, adult mice with normal growth continued to exhibit TH17-associated ileal crypt hyperplasia and additionally accumulated ileal-reactive Treg cells. Both IL-17A and IFNγ were protective, as their deficiency precluded ileal-reactive Treg accumulation and exacerbated colitic disease. IL-23R blockade prevented progression to colitis, whereas nTreg cell transfers prevented colitic disease, ileal crypt hyperplasia and ileal-reactive Treg accumulation. Thus, our studies identify an IL-17A and IFNγ-dependent homeostatic process that mobilizes ileal-reactive Treg cells and is disrupted by IL-23. More... »

PAGES

1127-1137

References to SciGraph publications

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41385-018-0023-6

    DOI

    http://dx.doi.org/10.1038/s41385-018-0023-6

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1103754034

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/29728642


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