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A possible interaction between periostin and CD 163 + skin‐resident macrophages in pemphigus vulgaris and bullous pemphigoid
Author(s) -
Fujimura Taku,
Kakizaki Aya,
Furudate Sadanori,
Aiba Setsuya
Publication year - 2017
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/exd.13157
Subject(s) - pemphigus vulgaris , periostin , bullous pemphigoid , chemokine , cytokine , immunology , pemphigoid , medicine , pathology , immune system , biology , antibody , extracellular matrix , microbiology and biotechnology
Pemphigus vulgaris ( PV ) and bullous pemphigoid ( BP ) are autoimmune blistering diseases, and substantial numbers of CD 163 + tissue‐associated macrophages ( TAM s) are detected in both diseases. PV and BP possess different subsets of helper T cells, suggesting that the cytokine profiles of PV and BP might be different. The purpose of this study was to investigate the microenvironment of lesional skin and serum of PV and BP patients, focusing on the immunomodulatory factors related to TAM s, such as periostin ( POSTN ), chemokines, cytokines and matrix metalloproteinases (MMPs). We first performed immunohistological staining of POSTN in PV and BP lesions. POSTN was prominent in the superficial dermis in both PV and BP lesions. Next, to validate the activation of CD 163 + TAM s in PV and BP patients, we examined the serum levels of soluble (s) CD 163. The serum sCD 163 levels in PV and BP patients are significantly higher than in healthy controls. To further elucidate the molecular mechanisms of the effects of POSTN on CD 163 + TAM s in PV and BP , we examined chemokines, MMPs and cytokines selected by DNA microarray database. The serum CXCL 5 levels from PV patients are significantly higher than those in BP patients and healthy controls. The IL ‐36γ expression on infiltrating macrophages was prominent only in the lesional skin of PV , while the MMP 12 deposition was detected in both PV and BP lesions. Our results shed light on the novel pathogenesis of PV through CD 163 + TAM s.