Inhibition of Mac-1 allows human macrophages to migrate against the direction of shear flow on ICAM-1.

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC
ACS Applied Electronic Materials Pub Date : 2024-10-01 Epub Date: 2024-08-21 DOI:10.1091/mbc.E24-03-0114
Aman Mittal, Subham Guin, Ai Mochida, Daniel A Hammer, Alexander Buffone
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引用次数: 0

Abstract

All immune cells must transit from the blood to distal sites such as the lymph nodes, bone marrow, or sites of infection. Blood borne monocytes traffic to the site of inflammation by adhering to the endothelial surface and migrating along endothelial intracellular adhesion molecule 1 (ICAM-1) by their ligand's macrophage 1 antigen (Mac-1) and lymphocyte functional antigen 1 (LFA-1) to transmigrate through the endothelium. Poor patient prognoses in chronic inflammation and tumors have been attributed to the hyper recruitment of certain types of macrophages. Therefore, targeting the binding of ICAM-1 to its respective ligands provides a novel approach to targeting the recruitment of macrophages. To that end, we determined whether the loss of Mac-1 expression could induce this upstream migration behavior by using blocking antibodies against Mac-1 to examine the effects of hydrodynamic flow on the migration of the human macrophage cell line U-937 on ICAM-1 surfaces. Blocking Mac-1 on U-937 cells led to upstream migration against the direction of shear flow on ICAM-1 surfaces. In sum, the ability of macrophages to migrate upstream when Mac-1 is blocked represents a new avenue to precisely control the differentiation, migration, and trafficking of macrophages.

抑制 Mac-1 可使人类巨噬细胞逆 ICAM-1 的剪切流方向迁移。
所有免疫细胞都必须从血液转移到远端部位,如淋巴结、骨髓或感染部位。血液中的单核细胞会粘附在内皮表面,并通过其配体巨噬细胞 1 抗原(Mac-1)和淋巴细胞功能抗原 1(LFA-1)沿内皮细胞内粘附分子 1(ICAM-1)迁移,从而通过内皮转运到炎症部位。慢性炎症和肿瘤患者预后不良的原因是某些类型的巨噬细胞过度招募。因此,靶向 ICAM-1 与其各自配体的结合为靶向巨噬细胞招募提供了一种新方法。为此,我们使用阻断 Mac-1 的抗体来检测流体力学流动对人巨噬细胞系 U-937 在 ICAM-1 表面迁移的影响,从而确定 Mac-1 的表达缺失是否会诱导这种上游迁移行为。总之,当 Mac-1 被阻断时,巨噬细胞能够向上游迁移,这为精确控制巨噬细胞的分化、迁移和贩运提供了一条新途径。[媒体:见正文] [媒体:见正文]。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
7.20
自引率
4.30%
发文量
567
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