IL-30 ameliorates imiquimod and K14-VEGF induced psoriasis-like disease by inhibiting both innate and adaptive immunity disorders.

Biochem Biophys Res Commun

State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, And Collaborative Innovation Center for Biotherapy, Chengdu, 610041, China. Electronic address:

Published: November 2021

AI Article Synopsis

  • Psoriasis is a serious skin condition that can negatively impact both physical and mental health, driven by immune system dysfunctions.
  • Research shows that interleukin (IL)-30 can inhibit key immune signals that contribute to psoriasis, leading to reduced inflammatory responses in skin cells and dendritic cells.
  • In studies, IL-30 not only decreased skin disease severity in laboratory models but also suggests potential as a treatment option for psoriasis.

Article Abstract

Psoriasis is a severe skin disease with significant physical and psychological health consequences. As a typical type of immune disease, both innate and adaptive immunity disorders play key roles in the development of psoriasis. Interleukin (IL)-30 was thought as a natural antagonist of gp130-mediated signaling that affects T helper type 1 and 17 cell polarization by inhibiting IL-6 and IL-27 signaling pathways. Here, we found that, in vitro, IL-30 reduced cytokine levels of HaCaT keratinocytes and dendritic cells (DCs), weakened the maturationS of DCs, inhibited DC-mediated T cell proliferation, and blocked the activation of nuclear factor-κB. In vivo, IL-30 inhibited the development of skin disease in two animal models: Krt14-Vegfa and imiquimod (IMQ)-induced psoriasis-like skin disease. Thus, IL-30 may be useful as a therapeutic agent for controlling psoriasis.

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Source
http://dx.doi.org/10.1016/j.bbrc.2021.09.042DOI Listing

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