The pruritogenic mediator endothelin-1 shifts the dendritic cell–T-cell response toward Th17/Th1 polarization

T. Nakahara, M. Kido-Nakahara, F. Ohno, D. Ulzii, T. Chiba, G. Tsuji, M. Furue

研究成果: ジャーナルへの寄稿学術誌査読

31 被引用数 (Scopus)

抄録

Endothelin-1 (ET-1) is associated with skin diseases such as atopic dermatitis (AD) and psoriasis. ET-1 is enhanced in the skin of patients AD and psoriasis. In addition, plasma levels of ET-1 are elevated in AD and psoriasis. Although both AD and psoriasis are T-cell–mediated skin diseases, the association between ET-1 and the T-cell immune response has not been clarified. To evaluate the role of ET-1 in inflammatory skin disease, we sought to investigate the effects of ET-1 on the functions of dendritic cells (DCs) and subsequent immune responses. For this purpose, we immunohistochemically confirmed the upregulation of ET-1 in the epidermis of patients with AD or psoriasis. ET-1 directly induced phenotypic maturation of bone marrow-derived DCs (BMDCs). In addition, ET-1 augmented the production of several cytokines and allogeneic stimulatory capacity of BMDCs. Interestingly, ET-1–activated BMDCs primed T cells to produce Th1 and Th17 cytokines, but not Th2 cytokines. These findings indicate that ET-1 polarizes the DC–T-cell response toward Th17/1 differentiation and may augment the persistent course of inflammatory skin diseases.

本文言語英語
ページ(範囲)511-515
ページ数5
ジャーナルAllergy: European Journal of Allergy and Clinical Immunology
73
2
DOI
出版ステータス出版済み - 2月 2018

!!!All Science Journal Classification (ASJC) codes

  • 免疫アレルギー学
  • 免疫学

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