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淋巴管内皮细胞 LTβR 信号控制免疫细胞的迁移。

LTβR Signaling Controls Lymphatic Migration of Immune Cells.

机构信息

Department of Surgery, University of Maryland School of Medicine, Baltimore, MD 21201, USA.

Center for Vascular and Inflammatory Diseases, University of Maryland School of Medicine, Baltimore, MD 21201, USA.

出版信息

Cells. 2021 Mar 29;10(4):747. doi: 10.3390/cells10040747.

DOI:10.3390/cells10040747
PMID:33805271
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8065509/
Abstract

The pleiotropic functions of lymphotoxin (LT)β receptor (LTβR) signaling are linked to the control of secondary lymphoid organ development and structural maintenance, inflammatory or autoimmune disorders, and carcinogenesis. Recently, LTβR signaling in endothelial cells has been revealed to regulate immune cell migration. Signaling through LTβR is comprised of both the canonical and non-canonical-nuclear factor κB (NF-κB) pathways, which induce chemokines, cytokines, and cell adhesion molecules. Here, we focus on the novel functions of LTβR signaling in lymphatic endothelial cells for migration of regulatory T cells (Tregs), and specific targeting of LTβR signaling for potential therapeutics in transplantation and cancer patient survival.

摘要

淋巴毒素 (LT)β 受体 (LTβR) 信号的多效性功能与次级淋巴器官的发育和结构维持、炎症或自身免疫性疾病以及肿瘤发生的控制有关。最近,内皮细胞中的 LTβR 信号被揭示可调节免疫细胞的迁移。LTβR 信号的传递包括经典和非经典核因子 κB (NF-κB) 途径,这些途径可诱导趋化因子、细胞因子和细胞黏附分子。在这里,我们重点关注 LTβR 信号在淋巴管内皮细胞中对调节性 T 细胞 (Treg) 迁移的新功能,以及针对 LTβR 信号的特定靶向治疗在移植和癌症患者生存中的潜在应用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b19/8065509/e558547abad7/cells-10-00747-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b19/8065509/c13afe693844/cells-10-00747-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b19/8065509/80c66bc2b155/cells-10-00747-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b19/8065509/c8dbdd51af7e/cells-10-00747-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b19/8065509/e558547abad7/cells-10-00747-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b19/8065509/c13afe693844/cells-10-00747-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b19/8065509/80c66bc2b155/cells-10-00747-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b19/8065509/c8dbdd51af7e/cells-10-00747-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b19/8065509/e558547abad7/cells-10-00747-g004.jpg

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Cholesterol restricts lymphotoxin β receptor-triggered NF-κB signaling.胆固醇限制淋巴毒素β受体触发的 NF-κB 信号转导。
CXCL12+ fibroblastic reticular cells in lymph nodes facilitate immune tolerance by regulating T cell-mediated alloimmunity.
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