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Corticotropin‐releasing factor decreases IL‐18 in the monocyte‐derived dendritic cell
Author(s) -
Lee Hee Jung,
Kwon Yeon Sook,
Park Chang Ook,
Oh Sang Ho,
Lee Ju Hee,
Wu Wen Hao,
Chang Nam Soo,
Lee MinGeol,
Lee Kwang Hoon
Publication year - 2009
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.2008.00781.x
Subject(s) - dendritic cell , immune system , atopic dermatitis , medicine , immunology , receptor , plasmacytoid dendritic cell , exacerbation , monocyte , corticotropin releasing hormone
Recent evidence suggests that crosstalk between mast cells, nerves and keratinocytes might be involved in the exacerbation of inflammatory conditions by stress, but the mechanism by which this occurs remains unclear. Corticotropin‐releasing factor (CRF), which activates the hypothalamo‐pituitary‐adrenal (HPA) axis under stress, also has pro‐inflammatory peripheral effects. However, there have been no reports about CRF receptor expression and the functional role of CRF in the dendritic cell (DC), which is considered to be the link between allergen uptake and the clinical manifestations of allergic diseases, such as atopic dermatitis. The purpose of this study was to investigate the expression of CRF receptors and the functional role of CRF in the monocyte‐derived DC (MoDC) of atopic dermatitis patients and non‐atopic healthy controls. In this study, mRNAs for CRF‐R1α and 1β, as well as the CRF‐R1 protein, were detected in MoDCs. CRF‐R2α (but not R2β or R2γ) mRNA and the CRF‐R2 protein were present in MoDCs. Exposure of DCs to CRF resulted in a decrease of IL‐18 in both atopic dermatitis patients and non‐atopic healthy controls. However, CRF did not alter the expression of IL‐6, CCL17, CCL18, and CCL22. Therefore, our results demonstrate that CRF could modulate immune responses by acting directly upon DCs.