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CD64 缺陷型小鼠狼疮血清诱导皮肤炎症的改善。

Amelioration of Lupus Serum-Induced Skin Inflammation in CD64-Deficient Mice.

机构信息

Department of Rheumatology and Immunology, Wuhan Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

出版信息

Front Immunol. 2022 Feb 22;13:824008. doi: 10.3389/fimmu.2022.824008. eCollection 2022.

DOI:10.3389/fimmu.2022.824008
PMID:35273604
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8901504/
Abstract

Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disorder characterized by high autoantibodies levels and multiorgan tissue damage. The current study investigated the role of CD64 in SLE patients and animal models. According to a flow cytometry study, SLE patients showed an increase in CD64 expression in circulating monocytes. There was a correlation between CD64 and SLEDAI, blood urea nitrogen levels, and anti-Sm antibodies. In skin lesions of lupus MRL/ mice, there was high IgG deposition and CD64 expression. , cytokines IL-10 and IFN-γ upregulated CD64 expression in monocytes/macrophages that was inhibited by glucocorticoids. In CD64-deficient mice, skin inflammation induced by lupus serum was reduced. Furthermore, activation of spleen tyrosine kinase (Syk), Akt, and extracellular signal-regulated kinase (Erk) was inhibited in CD64-deficient monocytes. The results suggest that CD64 could be a biomarker for observing SLE progression, as well as a mechanistic checkpoint in lupus pathogenesis.

摘要

系统性红斑狼疮（SLE）是一种异质性自身免疫性疾病，其特征是自身抗体水平高和多器官组织损伤。本研究探讨了 CD64 在 SLE 患者和动物模型中的作用。根据流式细胞术研究，SLE 患者循环单核细胞中 CD64 的表达增加。CD64 与 SLEDAI、血尿素氮水平和抗 Sm 抗体之间存在相关性。在狼疮 MRL/小鼠的皮肤损伤中，存在 IgG 的高沉积和 CD64 的表达。此外，细胞因子 IL-10 和 IFN-γ 上调了单核细胞/巨噬细胞中的 CD64 表达，而糖皮质激素则抑制了这种表达。在 CD64 缺陷型小鼠中，狼疮血清诱导的皮肤炎症减轻。此外，CD64 缺陷型单核细胞中脾酪氨酸激酶（Syk）、Akt 和细胞外信号调节激酶（Erk）的激活受到抑制。这些结果表明，CD64 可以作为观察 SLE 进展的生物标志物，也是狼疮发病机制中的一个机制检查点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/407f/8901504/a216e0ace40e/fimmu-13-824008-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/407f/8901504/673288af9f55/fimmu-13-824008-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/407f/8901504/8e1b1d72b9bc/fimmu-13-824008-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/407f/8901504/9d393f500e81/fimmu-13-824008-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/407f/8901504/89b3915514ee/fimmu-13-824008-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/407f/8901504/4bc25f8630c1/fimmu-13-824008-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/407f/8901504/a216e0ace40e/fimmu-13-824008-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/407f/8901504/673288af9f55/fimmu-13-824008-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/407f/8901504/8e1b1d72b9bc/fimmu-13-824008-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/407f/8901504/9d393f500e81/fimmu-13-824008-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/407f/8901504/89b3915514ee/fimmu-13-824008-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/407f/8901504/4bc25f8630c1/fimmu-13-824008-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/407f/8901504/a216e0ace40e/fimmu-13-824008-g006.jpg

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