Abstract

Psoriasis is a chronic inflammatory skin disease that is associated with multiple coexisting conditions. Extensive literature suggests that psoriasis is a T-cell-mediated condition, and its pathogenesis is related to dysfunction of the immune system. Myeloid-derived suppressor cells (MDSCs) are a group of heterogeneous myeloid cells that have suppressive effects on T cells. MDSCs are present at very low levels in healthy individuals but can substantially expand in tumours or inflammatory conditions. PSORI-CM02, a Chinese medical formula designed based on the Chinese medicine theory (Blood Stasis), has been prescribed extensively for psoriasis therapy and shows a stable clinical effect and safety. This study discusses the mechanisms of MDSCs involved in disease development and therapeutic progress. Our data provides evidence that monocytic myeloid-derived suppressor cells (M-MDSCs) play a role in IMQ-induced psoriatic dermatitis. Functional characterization and correlation analysis indicated that MDSCs are positively correlated with Th17 cells. PSORI-CM02 alleviated IMQ-induced psoriatic dermatitis and suppressed the proliferation of Th17 cells via M-MDSC-induced Arg1 upregulation, suggesting M-MDSCs could be a novel therapeutic target for psoriasis, and PSORI-CM02 exerted its effects via the perturbation of M-MDSCs and Th17 cell crosstalk.

Highlights

  • Psoriasis is a common skin disease caused by both autoimmune dysfunction and genetic burden

  • These results suggested that the Myeloid-derived suppressor cells (MDSCs), especially monocytic myeloid-derived suppressor cells (M-MDSCs), were involved in the pathological mechanism of IMQ-induced psoriatic dermatitis

  • To analyse the mechanism of PSORI-CM02 treatment effected on the psoriatic immune environment, we evaluated the M-MDSC markers (Arg1, TGFβ1, inducible nitric oxide synthase (iNOS), IL-10, and IL-13) and psoriatic inflammatory cytokines (Th1/Th2/Th17 cytokines) in skin samples of different groups by Cytometric Bead Array (CBA), Enzyme-Linked Immunosorbent Assay (ELISA) and RT-qPCR

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Summary

Introduction

Psoriasis is a common skin disease caused by both autoimmune dysfunction and genetic burden. The worldwide prevalence of psoriasis is estimated at approximately 2%, and the prevalence is in a diverse range according to regions (Parisi et al, 2013). Patients with psoriasis have been reported to suffer from elevated rates of various psychopathologies, including depression, anxiety, sexual dysfunction, poor self-esteem, and even suicidal ideation (Kimball et al, 2005; Kimball et al, 2012). Breakthroughs in the understanding of the pathogenesis of psoriasis have developed from its histopathologic accelerated cell proliferation of keratinocytes to the pathogenesis of chronic inflammatory with a dominant IL-23/Th17 axis (Zheng et al, 2007; Ogawa et al, 2018). The crosstalk within neutrophils, dendritic cells, T cells, and the cytokines released from immune cells are the central pathogenesis of psoriasis progress (Boehncke and Schon, 2015).

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