NDLI: Innate PI3K p110Î´ regulates Th1/Th17 development and microbiota-dependent colitis.

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Innate PI3K p110Î´ regulates Th1/Th17 development and microbiota-dependent colitis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Plevy, Scott E. Ting, Jenny P. Y. Kobayashi, Taku Russo, Steven M. Sheikh, Shehzad Z. Steinbach, Erin C. Uno, Jennifer K. Herfarth, Hans Mishima, Yoshiyuki Sartor, R. Balfour Liu, Bo Kennedy, Samantha T. Borst, Luke B. Gipson, Gregory R.
Description	Author Affiliation: Steinbach EC ( Department of Microbiology and Immunology, University of North Carolina School of Medicine, Chapel Hill, NC 27599)
Abstract	The p110Î´ subunit of class IA PI3K modulates signaling in innate immune cells. We previously demonstrated that mice harboring a kinase-dead p110Î´ subunit (p110Î´(KD)) develop spontaneous colitis. Macrophages contributed to the Th1/Th17 cytokine bias in p110Î´(KD) mice through increased IL-12 and IL-23 expression. In this study, we show that the enteric microbiota is required for colitis development in germfree p110Î´(KD) mice. Colonic tissue and macrophages from p110Î´(KD) mice produce significantly less IL-10 compared with wild-type mice. p110Î´(KD) APCs cocultured with naive CD4+ Ag-specific T cells also produce significantly less IL-10 and induce more IFN-Î³- and IL-17A-producing CD4+ T cells compared with wild-type APCs. Illustrating the importance of APC-T cell interactions in colitis pathogenesis in vivo, Rag1(-/-)/p110Î´(KD) mice develop mild colonic inflammation and produced more colonic IL-12p40 compared with Rag1(-/-) mice. However, CD4+ CD45RB(high/low) T cell Rag1(-/-)/p110Î´(KD) recipient mice develop severe colitis with increased percentages of IFN-Î³- and IL-17A-producing lamina propria CD3+D4+ T cells compared with Rag1(-/-) recipient mice. Intestinal tissue samples from patients with Crohn's disease reveal significantly lower expression of PIK3CD compared with intestinal samples from non-inflammatory bowel disease control subjects (p < 0.05). PIK3CD expression inversely correlates with the ratio of IL12B:IL10 expression. In conclusion, the PI3K subunit p110Î´ controls homeostatic APC-T cell interactions by altering the balance between IL-10 and IL-12/23. Defects in p110Î´ expression and/or function may underlie the pathogenesis of human inflammatory bowel disease and lead to new therapeutic strategies.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1301533
Journal	The Journal of Immunology
Issue Number	8
Volume Number	192
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-04-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Class Ia Phosphatidylinositol 3-kinase Metabolism Colitis Immunology Immunity, Innate Th1 Cells Th17 Cells Animals Antigen-presenting Cells Genetics Microbiology Pathology Cytokines Biosynthesis Disease Models, Animal Gene Expression Regulation Interleukin-10 Intestinal Mucosa Macrophages Mice Mice, Knockout Microbiota Tor Serine-threonine Kinases Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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