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

Document Type

Article

Publication Date

10-1-2024

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.

Identifier

85204661001 (Scopus)

Publication Title

Molecular Biology of the Cell

External Full Text Location

https://doi.org/10.1091/mbc.E24-03-0114

e-ISSN

19394586

ISSN

10591524

PubMed ID

39167496

Issue

10

Volume

35

Grant

GM143357

Fund Ref

National Institute of General Medical Sciences

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