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VSIG4 的生物学特性:在免疫介导的炎症性疾病和癌症治疗中的意义。

The biology of VSIG4: Implications for the treatment of immune-mediated inflammatory diseases and cancer.

机构信息

Department of Hematology, The Fifth Medical Center of PLA General Hospital, Beijing, 100071, China; PLA 307 Clinical College of Anhui Medical University, Beijing, 100071, China.

Department of Hematology, The Fifth Medical Center of PLA General Hospital, Beijing, 100071, China.

出版信息

Cancer Lett. 2023 Jan 28;553:215996. doi: 10.1016/j.canlet.2022.215996. Epub 2022 Nov 5.

DOI:10.1016/j.canlet.2022.215996
PMID:36343787
Abstract

V-set and immunoglobulin domain containing 4 (VSIG4), a type I transmembrane receptor exclusively expressed in a subset of tissue-resident macrophages, plays a pivotal role in clearing C3-opsonized pathogens and their byproducts from the circulation. VSIG4 maintains immune homeostasis by suppressing the activation of complement pathways or T cells and inducing regulatory T-cell differentiation, thereby inhibiting the development of immune-mediated inflammatory diseases but enhancing cancer progression. Consequently, VSIG4 exhibits a potential therapeutic effect for immune-mediated inflammatory diseases, but also is regarded as a novel target of immune checkpoint inhibition in cancer therapy. Recently, soluble VSIG4, the extracellular domain of VSIG4, shed from the surface of macrophages, has been found to be a biomarker to define macrophage activation-related diseases. This review mainly summarizes recent new findings of VSIG4 in macrophage phagocytosis and immune homeostasis, and discusses its potential diagnostic and therapeutic usage in infection, inflammation, and cancer.

摘要

V -set 和免疫球蛋白结构域蛋白 4(VSIG4)是一种仅在一组组织驻留巨噬细胞中表达的 I 型跨膜受体,在清除补体 C3 调理的病原体及其产物方面发挥着关键作用。VSIG4 通过抑制补体途径或 T 细胞的激活以及诱导调节性 T 细胞分化来维持免疫稳态,从而抑制免疫介导的炎症性疾病的发展,但促进癌症的进展。因此,VSIG4 对免疫介导的炎症性疾病具有潜在的治疗作用,但也被认为是癌症治疗中免疫检查点抑制的新靶点。最近,发现巨噬细胞表面脱落的可溶性 VSIG4(VSIG4 的细胞外结构域)是定义与巨噬细胞活化相关疾病的生物标志物。本文主要总结了 VSIG4 在巨噬细胞吞噬作用和免疫稳态方面的最新新发现,并讨论了其在感染、炎症和癌症中的潜在诊断和治疗用途。

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Cancer Lett. 2023 Jan 28;553:215996. doi: 10.1016/j.canlet.2022.215996. Epub 2022 Nov 5.
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