TY - JOUR
T1 - Minocycline decreases Th2 chemokines from M2 macrophages
T2 - Possible mechanisms for the suppression of bullous pemphigoid by traditional bullous disease drugs
AU - Tanita, Kayo
AU - Fujimura, Taku
AU - Sato, Yota
AU - Lyu, Chunbing
AU - Aiba, Setsuya
N1 - Funding Information:
This study was supported in part by a
Publisher Copyright:
© 2018 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
PY - 2018/11
Y1 - 2018/11
N2 - 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 CD163+ M2 macrophages in vitro, with special focus on the production of CCL18 and CCL22, both of which are produced by CD163+ M2 macrophages in the lesional skin of BP and are increased in the serum of BP patients. Minocycline decreased the production of CCL22, CCL24 and CCL26 as well as CCL2 from M2 macrophages. CCL18 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.
AB - 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 CD163+ M2 macrophages in vitro, with special focus on the production of CCL18 and CCL22, both of which are produced by CD163+ M2 macrophages in the lesional skin of BP and are increased in the serum of BP patients. Minocycline decreased the production of CCL22, CCL24 and CCL26 as well as CCL2 from M2 macrophages. CCL18 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.
KW - CCL22
KW - bullous pemphigoid
KW - minocycline/tetracycline
KW - tissue-associated macrophages
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U2 - 10.1111/exd.13779
DO - 10.1111/exd.13779
M3 - Article
C2 - 30192415
AN - SCOPUS:85054572509
VL - 27
SP - 1268
EP - 1272
JO - Experimental Dermatology
JF - Experimental Dermatology
SN - 0906-6705
IS - 11
ER -