The two faces of mast cells in vitiligo pathogenesis-Reference-Cited by-同舟云学术

The two faces of mast cells in vitiligo pathogenesis

Published:2021-10-08 Issue: Volume: Page:
ISSN:2768-6655
Container-title:Exploration of Immunology
language:en
Short-container-title:Explor Immunol

Author:

Katayama Ichiro¹,Yang Lingli¹,Takahashi Aya²,Yang Fei¹,Wataya-Kaneda Mari³

Affiliation:

1. 1Department of Dermatology, Graduate School of Medicine, Osaka University, Suita, Osaka 5650871, Japan 2Department of Pigmentation Research and Therapeutics, Graduate School of Medicine, Osaka City University, Osaka 5450051, Japan

2. 1Department of Dermatology, Graduate School of Medicine, Osaka University, Suita, Osaka 5650871, Japan

3. Department of Dermatology, Graduate School of Medicine, Osaka University, Suita, Osaka 5650871, Japan

Abstract

Aim: Previously, we reported increased number of T helper 17 (Th17) cells in vitiligo. However, in our recent study, tryptase and interleukin (IL)17 double positive cells which identified by polyclonal anti-IL17 antibody with specificity for IL17A, B, D, F was observed, but these mast cells cannot be stained by monoclonal anti-IL17 antibody with specificity for IL17A. Therefore, this study was aimed to clarify the role of mast cells in induction and progression of vitiligo. Methods: Mast cells were stained with two antibodies against IL17 and one antibody against tryptase by immunofluorescent staining. Furthermore, immunoelectron microscopy (IEM) analyses were conducted using anti-tryptase. In vitro, cultured epidermal keratinocytes were treated with agents which released by mast cells. Expression levels of mRNA were analyzed by real-time polymerase chain reaction (PCR), expression of protein levels was analyzed by western blotting. Results: An increased number of tryptase positive mast cells was observed at the lesional skin of upper dermis in vitiligo and rhododendrol-induced leukoderma (RDIL). These mast cells showed prominent degranulation in vitiligo. Interestingly, the melanosome forming glycoprotein non-metastatic melanoma protein B (GPNMB) is downregulated in the lesional basal keratinocytes in vitiligo and mast cell tryptase contributes to this phenomenon. In addition, small interfering GPNMB RNA (siGPNMB RNA)-introduced keratinocytes increased melanocyte survival through stem cell factor (SCF) production in the melanocyte/keratinocyte co-culture system. Conclusions: Mast cells might be two-faced in vitiligo induction, progression, and recovery through the differential function of histamine and tryptase.

Publisher

Open Exploration Publishing

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