The two faces of mast cells in vitiligo pathogenesis

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 b...

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Autores principales: Ichiro Katayama, Lingli Yang, Aya Takahashi, Fei Yang, Mari Wataya-Kaneda
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Publicado: Open Exploration Publishing Inc. 2021
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spelling oai:doaj.org-article:bb2aecab03c042e98034b6788300bf412021-11-24T06:38:07ZThe two faces of mast cells in vitiligo pathogenesis10.37349/ei.2021.000182768-6655https://doaj.org/article/bb2aecab03c042e98034b6788300bf412021-10-01T00:00:00Zhttps://www.explorationpub.com/Journals/ei/Article/100318https://doaj.org/toc/2768-6655Aim: 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.Ichiro KatayamaLingli YangAya TakahashiFei YangMari Wataya-KanedaOpen Exploration Publishing Inc.articlevitiligorhododendrol-induced leukodermamast celltryptaseinterleukin 17Immunologic diseases. AllergyRC581-607ENExploration of Immunology, Vol 1, Iss 4, Pp 269-284 (2021)
institution DOAJ
collection DOAJ
language EN
topic vitiligo
rhododendrol-induced leukoderma
mast cell
tryptase
interleukin 17
Immunologic diseases. Allergy
RC581-607
spellingShingle vitiligo
rhododendrol-induced leukoderma
mast cell
tryptase
interleukin 17
Immunologic diseases. Allergy
RC581-607
Ichiro Katayama
Lingli Yang
Aya Takahashi
Fei Yang
Mari Wataya-Kaneda
The two faces of mast cells in vitiligo pathogenesis
description 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.
format article
author Ichiro Katayama
Lingli Yang
Aya Takahashi
Fei Yang
Mari Wataya-Kaneda
author_facet Ichiro Katayama
Lingli Yang
Aya Takahashi
Fei Yang
Mari Wataya-Kaneda
author_sort Ichiro Katayama
title The two faces of mast cells in vitiligo pathogenesis
title_short The two faces of mast cells in vitiligo pathogenesis
title_full The two faces of mast cells in vitiligo pathogenesis
title_fullStr The two faces of mast cells in vitiligo pathogenesis
title_full_unstemmed The two faces of mast cells in vitiligo pathogenesis
title_sort two faces of mast cells in vitiligo pathogenesis
publisher Open Exploration Publishing Inc.
publishDate 2021
url https://doaj.org/article/bb2aecab03c042e98034b6788300bf41
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