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- W2075133023 abstract "Abstract Background Prolactin (PRL) is a pituitary‐derived neuropeptide hormone that has been suggested to promote the development of psoriasis, a Th17/Th1‐mediated inflammatory dermatosis. PRL increases the expression of Th1 cytokines; however, its effects on Th17 responses are unknown. Objective This study aims to determine the in vivo effects of PRL on the expression of Th17 cytokines/chemokines in imiquimod‐induced psoriasiform skin inflammation in mice. Methods BALB/c mice were intraperitoneally injected with PRL or phosphate‐buffered saline, and imiquimod cream or Vaseline was applied to the shaved back skin for six consecutive days. Results Intraperitoneal PRL increased the mRNA levels of IL‐17A, IL‐17F, IL‐22, IL‐23p19, IL‐12p40, CCL20 and STAT3 in imiquimod‐treated skin. Mice treated with imiquimod plus PRL, but not those treated with imiquimod plus phosphate‐buffered saline, showed significantly increased mRNA levels of TNF‐α, IFN‐γ, IL‐12p35 and CXCL2 compared with controls. Intraperitoneal PRL increased the numbers of CD3 + and GR‐1 + cells in the dermis of imiquimod‐treated skin. Conclusions These results suggest that intraperitoneal PRL enhances the expression of Th17 and Th1 cytokines/chemokines, and augments inflammation in imiquimod‐induced psoriasiform skin. Prolactin may thus exacerbate psoriasis through the enhancement of Th17/Th1 responses." @default.
- W2075133023 created "2016-06-24" @default.
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- W2075133023 date "2013-11-07" @default.
- W2075133023 modified "2023-10-02" @default.
- W2075133023 title "Prolactin induces the production of Th17 and Th1 cytokines/chemokines in murine Imiquimod-induced psoriasiform skin" @default.
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- W2075133023 doi "https://doi.org/10.1111/jdv.12295" @default.
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