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J Immunol. 2016 Jan 15;196(2):543-6. doi: 10.4049/jimmunol.1502080. Epub 2015 Dec 7.

Cutting Edge: IL-1 Receptor Signaling is Critical for the Development of Autoimmune Uveitis.

Author information

1
Laboratory of Molecular Immunology and the Immunology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892; and.
2
Molecular Immunology Section, National Eye Institute, National Institutes of Health, Bethesda, MD 20892.
3
Molecular Immunology Section, National Eye Institute, National Institutes of Health, Bethesda, MD 20892 wjl@helix.nih.gov egwuaguc@nei.nih.gov.
4
Laboratory of Molecular Immunology and the Immunology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892; and wjl@helix.nih.gov egwuaguc@nei.nih.gov.

Abstract

IL-1β is a proinflammatory cytokine important for local and systemic immunity. However, aberrant production of this cytokine is implicated in pathogenic mechanisms of a number of inflammatory diseases, including Behçet's disease and age-related macular degeneration. In this study, we report the increased secretion of IL-1β in the retina by neutrophils, macrophages, and dendritic cells during ocular inflammation and show that loss of IL-1R signaling confers protection from experimental autoimmune uveitis. Moreover, the amelioration of experimental autoimmune uveitis in Il1r-deficient mice was associated with reduced infiltration of inflammatory cells into the retina and decreased numbers of uveitogenic Th17 cells that mediate uveitis. These findings indicate the possible utility of IL-1R-blocking agents for the treatment of ocular inflammatory diseases.

PMID:
26643477
PMCID:
PMC4707108
DOI:
10.4049/jimmunol.1502080
[Indexed for MEDLINE]
Free PMC Article

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