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Minocycline decreases Th2 chemokines from M2 macrophages: Possible mechanisms for the suppression of bullous pemphigoid by traditional bullous disease drugs
Author(s) -
Tanita Kayo,
Fujimura Taku,
Sato Yota,
Lyu Chunbing,
Aiba Setsuya
Publication year - 2018
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.13779
Subject(s) - minocycline , dexamethasone , bullous pemphigoid , medicine , tetracycline , chemokine , immunology , doxycycline , acne , pharmacology , inflammation , dermatology , chemistry , antibiotics , antibody , biochemistry
Minocycline/tetracycline is clinically used for the treatment of bullous pemphigoid ( BP ), and its clinical benefits are superior to those of prednisolone when considering adverse events. Although the clinical benefits of minocycline/tetracycline are well known, its immunosuppressive mechanisms are still unclear. In this study, we investigated the immunomodulatory effects of traditional anti‐ BP drugs (minocycline, nicotinic acid amide, dexamethasone and cyclosporine) on CD 163 + M2 macrophages in vitro, with special focus on the production of CCL 18 and CCL 22, both of which are produced by CD 163 + M2 macrophages in the lesional skin of BP and are increased in the serum of BP patients. Minocycline decreased the production of CCL 22, CCL 24 and CCL 26 as well as CCL 2 from M2 macrophages. CCL 18 from M2 macrophages was decreased by dexamethasone and cyclosporine, but not decreased by minocycline. These data suggest that the clinical benefit of minocycline is partially explained by its suppressive effects against the production of specific Th2 chemokines from M2 macrophages, which should contribute to the recruitment of Th2 cells and eosinophils in the lesional skin of BP patients.