Prolactin induces the production of Th17 and Th1 cytokines/chemokines in murine Imiquimod-induced psoriasiform skin


  • Conflicts of interest

    • None declared.
  • Funding sources

    • This work was supported by a grant from the Japan Society for the Promotion of Science (18244120 to N. Kanda).



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.


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.


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.


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.


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.