Corticotropin-releasing hormone downregulates IL-10 production by adaptive forkhead box protein 3-negative regulatory T cells in patients with atopic dermatitis

SangHo Oh, Chang Ook Park, Wen Hao Wu, Ji Young Kim, Shan Jin, Dashlkhumbe Byamba, Byung Gi Bae, Seongmin Noh, Beom Jin Lim, Ji Yeon Noh, Kwanghoon Lee

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

Background: Corticotropin-releasing hormone (CRH) is the central regulating hormone of the hypothalamic-pituitary-adrenal axis. CRH also has diverse functional effects in the periphery and is related to the aggravation of several cutaneous diseases; however, the effect of CRH on T cells in patients with atopic dermatitis (AD) has not been well evaluated. Objective: We investigated whether CRH directly affects peripheral T H 1, T H 2, and regulatory T (Treg) cells in patients with AD. Methods: We assessed whether T cells express the CRH receptor protein and mRNA by using flow cytometry, Western blotting, immunofluorescence, immunohistochemistry, and RT-PCR. We evaluated cytokine expression using ELISA after treating the T cells extracted from patients with AD and healthy control subjects (HCs) with CRH. Flow cytometry was then used to evaluate any direct effects of CRH on T H 1, T H 2, and Treg cells from patients with AD and HCs. Results: T cells from patients with AD expressed significantly lower CRH receptor 1/2 mRNA levels than T cells from HCs. T cells from HCs reacted with different IL-4 and IFN-γ secretions to CRH treatment, whereas T cells from patients with AD did not. IL-10 production was significantly decreased in the supernatants from both the HCs and patients with AD after CRH treatment. CRH upregulated IL-4 production by T H 2 cells and downregulated IFN-γ production by T H 1 cells in HCs. CRH also suppressed the production of IL-10 by forkhead box protein 3-negative Treg cells in both groups, but the difference was only significant in patients with AD. Conclusions: CRH-mediated suppression of IL-10 secretion from Treg cells might explain stress-related exacerbations in patients with AD.

Original languageEnglish
JournalJournal of Allergy and Clinical Immunology
Volume129
Issue number1
DOIs
Publication statusPublished - 2012 Jan 1

Fingerprint

Forkhead Transcription Factors
Corticotropin-Releasing Hormone
Regulatory T-Lymphocytes
Atopic Dermatitis
Interleukin-10
Down-Regulation
T-Lymphocytes
Corticotropin-Releasing Hormone Receptors
Interleukin-4
Flow Cytometry
Hypothalamic Hormones
Messenger RNA
Skin Diseases
Fluorescent Antibody Technique
Healthy Volunteers
Western Blotting
Enzyme-Linked Immunosorbent Assay
Immunohistochemistry

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

Cite this

Oh, SangHo ; Park, Chang Ook ; Wu, Wen Hao ; Kim, Ji Young ; Jin, Shan ; Byamba, Dashlkhumbe ; Bae, Byung Gi ; Noh, Seongmin ; Lim, Beom Jin ; Noh, Ji Yeon ; Lee, Kwanghoon. / Corticotropin-releasing hormone downregulates IL-10 production by adaptive forkhead box protein 3-negative regulatory T cells in patients with atopic dermatitis. In: Journal of Allergy and Clinical Immunology. 2012 ; Vol. 129, No. 1.
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abstract = "Background: Corticotropin-releasing hormone (CRH) is the central regulating hormone of the hypothalamic-pituitary-adrenal axis. CRH also has diverse functional effects in the periphery and is related to the aggravation of several cutaneous diseases; however, the effect of CRH on T cells in patients with atopic dermatitis (AD) has not been well evaluated. Objective: We investigated whether CRH directly affects peripheral T H 1, T H 2, and regulatory T (Treg) cells in patients with AD. Methods: We assessed whether T cells express the CRH receptor protein and mRNA by using flow cytometry, Western blotting, immunofluorescence, immunohistochemistry, and RT-PCR. We evaluated cytokine expression using ELISA after treating the T cells extracted from patients with AD and healthy control subjects (HCs) with CRH. Flow cytometry was then used to evaluate any direct effects of CRH on T H 1, T H 2, and Treg cells from patients with AD and HCs. Results: T cells from patients with AD expressed significantly lower CRH receptor 1/2 mRNA levels than T cells from HCs. T cells from HCs reacted with different IL-4 and IFN-γ secretions to CRH treatment, whereas T cells from patients with AD did not. IL-10 production was significantly decreased in the supernatants from both the HCs and patients with AD after CRH treatment. CRH upregulated IL-4 production by T H 2 cells and downregulated IFN-γ production by T H 1 cells in HCs. CRH also suppressed the production of IL-10 by forkhead box protein 3-negative Treg cells in both groups, but the difference was only significant in patients with AD. Conclusions: CRH-mediated suppression of IL-10 secretion from Treg cells might explain stress-related exacerbations in patients with AD.",
author = "SangHo Oh and Park, {Chang Ook} and Wu, {Wen Hao} and Kim, {Ji Young} and Shan Jin and Dashlkhumbe Byamba and Bae, {Byung Gi} and Seongmin Noh and Lim, {Beom Jin} and Noh, {Ji Yeon} and Kwanghoon Lee",
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Corticotropin-releasing hormone downregulates IL-10 production by adaptive forkhead box protein 3-negative regulatory T cells in patients with atopic dermatitis. / Oh, SangHo; Park, Chang Ook; Wu, Wen Hao; Kim, Ji Young; Jin, Shan; Byamba, Dashlkhumbe; Bae, Byung Gi; Noh, Seongmin; Lim, Beom Jin; Noh, Ji Yeon; Lee, Kwanghoon.

In: Journal of Allergy and Clinical Immunology, Vol. 129, No. 1, 01.01.2012.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Corticotropin-releasing hormone downregulates IL-10 production by adaptive forkhead box protein 3-negative regulatory T cells in patients with atopic dermatitis

AU - Oh, SangHo

AU - Park, Chang Ook

AU - Wu, Wen Hao

AU - Kim, Ji Young

AU - Jin, Shan

AU - Byamba, Dashlkhumbe

AU - Bae, Byung Gi

AU - Noh, Seongmin

AU - Lim, Beom Jin

AU - Noh, Ji Yeon

AU - Lee, Kwanghoon

PY - 2012/1/1

Y1 - 2012/1/1

N2 - Background: Corticotropin-releasing hormone (CRH) is the central regulating hormone of the hypothalamic-pituitary-adrenal axis. CRH also has diverse functional effects in the periphery and is related to the aggravation of several cutaneous diseases; however, the effect of CRH on T cells in patients with atopic dermatitis (AD) has not been well evaluated. Objective: We investigated whether CRH directly affects peripheral T H 1, T H 2, and regulatory T (Treg) cells in patients with AD. Methods: We assessed whether T cells express the CRH receptor protein and mRNA by using flow cytometry, Western blotting, immunofluorescence, immunohistochemistry, and RT-PCR. We evaluated cytokine expression using ELISA after treating the T cells extracted from patients with AD and healthy control subjects (HCs) with CRH. Flow cytometry was then used to evaluate any direct effects of CRH on T H 1, T H 2, and Treg cells from patients with AD and HCs. Results: T cells from patients with AD expressed significantly lower CRH receptor 1/2 mRNA levels than T cells from HCs. T cells from HCs reacted with different IL-4 and IFN-γ secretions to CRH treatment, whereas T cells from patients with AD did not. IL-10 production was significantly decreased in the supernatants from both the HCs and patients with AD after CRH treatment. CRH upregulated IL-4 production by T H 2 cells and downregulated IFN-γ production by T H 1 cells in HCs. CRH also suppressed the production of IL-10 by forkhead box protein 3-negative Treg cells in both groups, but the difference was only significant in patients with AD. Conclusions: CRH-mediated suppression of IL-10 secretion from Treg cells might explain stress-related exacerbations in patients with AD.

AB - Background: Corticotropin-releasing hormone (CRH) is the central regulating hormone of the hypothalamic-pituitary-adrenal axis. CRH also has diverse functional effects in the periphery and is related to the aggravation of several cutaneous diseases; however, the effect of CRH on T cells in patients with atopic dermatitis (AD) has not been well evaluated. Objective: We investigated whether CRH directly affects peripheral T H 1, T H 2, and regulatory T (Treg) cells in patients with AD. Methods: We assessed whether T cells express the CRH receptor protein and mRNA by using flow cytometry, Western blotting, immunofluorescence, immunohistochemistry, and RT-PCR. We evaluated cytokine expression using ELISA after treating the T cells extracted from patients with AD and healthy control subjects (HCs) with CRH. Flow cytometry was then used to evaluate any direct effects of CRH on T H 1, T H 2, and Treg cells from patients with AD and HCs. Results: T cells from patients with AD expressed significantly lower CRH receptor 1/2 mRNA levels than T cells from HCs. T cells from HCs reacted with different IL-4 and IFN-γ secretions to CRH treatment, whereas T cells from patients with AD did not. IL-10 production was significantly decreased in the supernatants from both the HCs and patients with AD after CRH treatment. CRH upregulated IL-4 production by T H 2 cells and downregulated IFN-γ production by T H 1 cells in HCs. CRH also suppressed the production of IL-10 by forkhead box protein 3-negative Treg cells in both groups, but the difference was only significant in patients with AD. Conclusions: CRH-mediated suppression of IL-10 secretion from Treg cells might explain stress-related exacerbations in patients with AD.

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