Journal
JOURNAL OF IMMUNOLOGY
Volume 201, Issue 4, Pages 1267-1274Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1800484
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Funding
- American Heart Association Scientist Development Grant [14SDG18700043]
- National Institute of General Medical Sciences of the National Institutes of Health [P20GM103447]
- National Institute of Allergy and Infectious Diseases of the National Institutes of Health [A199F, 5 U19 AI062629, A179F]
- Oklahoma Center for the Advancement for Science and Technology Health Research Grant [HR 13-003]
- Oklahoma Center for Adult Stem Cell Research grant, a program of the Oklahoma Tobacco Settlement Endowment Trust
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Glucocorticoids (GCs) are commonly prescribed to patients with a variety of inflammatory disorders, including inflammatory bowel disease (IBD). GCs mediate their immunomodulatory effects through many different mechanisms and target multiple signaling pathways. The GC dexamethasone downmodulates innate and adaptive immune cell activation. IBD is the manifestation of a dysregulated immune response involving many different immune cells. Group 3 innate lymphocytes (ILC3s) have critical roles in mucosal inflammation. ILC3s secrete high levels of the cytokine IL-22, promoting epithelial proliferation, antimicrobial peptides, and mucins. In this study, we examined the effects of dexamethasone on IL-22 production by ILC3s. We found that dexamethasone suppressed IL-23-mediated IL-22 production in human and mouse ILC3s. This was mediated in part through dexamethasone modulation of the NF-kappa B pathway. Inhibition of NF-kappa B signaling with a small molecule inhibitor also downmodulated IL-23- and IL-1 beta-mediated IL-22 production in ILC3s. These findings implicate NF-kappa B as a regulator of IL-22 in ILC3s and likely have repercussions on GC treatment of IBD patients.
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