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CD200-CD200R1 signalling attenuates imiquimod-induced psoriatic inflammation by inhibiting the activation of skin inflammatory macrophages.

Abstract：

:Psoriasis is an autoimmune skin disease caused by interactions between keratinocytes and immune cells, such as macrophages. CD200 is expressed on the surface of various cell types, and its receptor, CD200R1, belongs to a family of immunosuppressive receptors that are mainly expressed on myeloid cells. CD200/CD200R1 signalling is associated with the prevention of autoimmune diseases; however, the role of CD200/CD200R1 signalling in the pathogenesis of psoriasis remains unknown. In this study, we detected in vivo effect of the CD200 protein on psoriasis and in vitro effects of CD200 on macrophages and keratinocytes co-cultured with macrophages were also evaluated. Our data showed that the expression of CD200 and CD200R1 was decreased and the expression of macrophage-related pro-inflammatory factors (IL-6, IL-1β, TNF-α) was increased in IMQ-induced psoriasis-like skin of mice. After subcutaneous injection of CD200, the symptoms were alleviated, local expression of CD200R1 was markedly induced, infiltrated CD68+ cells were significantly reduced and the expression levels of IL-6, IL-1β, and TNF-α were strongly downregulated. In in vitro experiments, CD200 suppressed the migration of macrophages, induced CD200R1 expression on the surface of macrophages, and decreased the levels of pro-inflammatory factors. Western blot (WB) data showed that the CD200-CD200R1 reaction controlled the activation of inflammatory macrophages by inhibiting the NF-κB signalling pathway. These results demonstrate that CD200-CD200R1 signalling can reduce IMQ-induced psoriasis-like skin inflammation by inhibiting the activation of macrophages.

journal_name

Int Immunopharmacol

journal_title

International immunopharmacology

authors

Li D,Wang Y,Tang L,Jin X,Xia C,Xu H,Hu J

doi

10.1016/j.intimp.2019.106046

subject

Has Abstract

pub_date

2020-01-01 00:00:00

pages

106046

eissn

1567-5769

issn

1878-1705

pii

S1567-5769(19)31955-1

journal_volume

78

pub_type

杂志文章

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