Clinical efficiency of topical calcipotriol/betamethasone treatment in psoriasis relies on suppression of the inflammatory TNFα – IL- 23 – IL-17 axis
Kubin, Minna E.; Kokkonen, Nina; Palatsi, Riitta; Hägg, Päivi M.; Väyrynen, Juha P.; Glumoff, Virpi; Haapasaari, Kirsi-Maria; Hurskainen, Tiina; Tasanen, Kaisa (2016-11-21)
Minna E. Kubin, Nina Kokkonen, Riitta Palatsi, Päivi M. Hägg, Juha P. Väyrynen, Virpi Glumoff, Kirsi-Maria Haapasaari, Tiina Hurskainen, Kaisa Tasanen. Clinical efficiency of topical calcipotriol/betamethasone treatment in psoriasis relies on suppression of the inflammatory TNFα – IL- 23 – IL-17 axis. Acta Derm Venereol 2017; 97: 449–455. doi: 10.2340/00015555-2579
Journal Compilation © 2017 Acta Dermato-Venereologica. This is an open access article under the CC BY-NC license.
https://creativecommons.org/licenses/by-nc/4.0/
https://urn.fi/URN:NBN:fi-fe201707047628
Tiivistelmä
Abstract
The effects of topical calcipotriol/betamethasone combination therapy and betamethasone monotherapy on inflammatory T-cell numbers and molecular markers were compared in patients with psoriasis. Combination therapy down-regulated the expression of tumour necrosis factor (TNF)-α, interleukin (IL)-23A, IL-17A, S100A7, CCL-20 and interferon (IFN)-γ in skin and TNF-α, IL-6, IL-23A, T-bet and IFN-γ in peripheral blood mononuclear cells (PBMCs). Betamethasone monotherapy had less effect. Expression of FoxP3 in both skin and PBMCs was down-regulated by calcipotriol/betamethasone, but not by betamethasone. Immunohistochemical analysis revealed that calcipotriol/betamethasone reduced the numbers of CD4+ and CD8+ T cells and Tregs in psoriatic lesions more than betamethasone. Flow cytometric analyses demonstrated that calcipotriol/betamethasone decreased the numbers of circulating CD8+ T cells, Tregs, skin-homing Th17 memory cells and Th22 memory cells, while betamethasone had little or no effect. Glucocorticoid receptors GRα and GRß were expressed in psoriatic skin. In conclusion, calcipotriol increases the immunosuppressive power of betamethasone by suppressing the inflammatory TNF-α – IL-23 – IL-17 axis.
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