Journal
INTERNATIONAL IMMUNOLOGY
Volume 25, Issue 6, Pages 335-343Publisher
OXFORD UNIV PRESS
DOI: 10.1093/intimm/dxt011
Keywords
dioxin receptor; immune regulation
Categories
Funding
- Japan Society for the Promotion of Science [24790471]
- National Institute of Biomedical Innovation
- Grants-in-Aid for Scientific Research [24790471] Funding Source: KAKEN
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A number of recent studies have examined the functions of aryl hydrocarbon receptor (Ahr) in the immune system. Also known as dioxin receptor, Ahr is a ligand-activated transcription factor that serves as a receptor for various environmental toxins. The functions of Ahr in T cells depend on the specific ligand bound to the receptor. For instance, binding of 2,3,7,8-tetrachlorodibenzo-p-dioxin to Ahr suppresses experimental autoimmune encephalomyelitis (EAE) by promoting the development of Foxp3(+) T-reg cells, whereas 6-formylindolo[3,2-b] carbazole enhances EAE by inducing the differentiation of IL-17-producing T cells. Furthermore, specifically deleting Ahr in T cells inhibits collagen-induced arthritis in mice. In macrophages and dendritic cells (DCs), Ahr is anti-inflammatory. In response to LPS, Ahr-deficient macrophages show increased production of pro-inflammatory cytokines, such as IL-6 and TNF-alpha, and Ahr-deficient DCs produce less of the anti-inflammatory cytokine IL-10. In this review, we discuss the roles of Ahr in macrophages and T cells. Moreover, studies examining Ahr activation in other cell types have revealed additional contributions to B cell and osteoblast/osteoclast differentiation. We also briefly summarize the current understanding of regulatory mechanisms underlying Ahr activation in various cells and discuss the potential clinical implications of cell-specific targeting of Ahr in pathologic conditions of the immune system.
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