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Assessment of Lymphocyte Migration in an Ex Vivo Transmigration System

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Published on: September 20, 2019

Endothelial cell-derived chemerin promotes dendritic cell transmigration.

Safiye Gonzalvo-Feo¹, Annalisa Del Prete, Monika Pruenster

¹Humanitas Clinical and Research Center, Rozzano 20089, Italy;

Journal of Immunology (Baltimore, Md. : 1950)

|January 29, 2014

Summary

Retinoic acid stimulates endothelial cells to produce chemerin, enhancing dendritic cell migration via the ChemR23 receptor. This interaction is crucial for immune cell trafficking in autoimmune conditions.

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Area of Science:

Immunology
Cell Biology
Vascular Biology

Background:

ChemR23 (chemoattractant receptor) is expressed by antigen-presenting cells (APCs) like dendritic cells.
Chemerin, the ChemR23 ligand, is linked to inflamed endothelial cells in autoimmune diseases.
Endothelial cells play a role in immune cell recruitment.

Purpose of the Study:

To investigate the role of endothelial cells in chemerin-mediated dendritic cell migration.
To determine the factors that induce endothelial chemerin production.
To elucidate the mechanisms by which activated endothelial cells influence dendritic cell transmigration.

Main Methods:

Murine endothelial cells were stimulated with retinoic acid and other factors.
Dendritic cell adhesion and transmigration assays were performed under shear stress.
Immunohistochemistry and flow cytometry were used to analyze receptor expression and protein localization.

Main Results:

Retinoic acid, but not proinflammatory cytokines, induced chemerin production in blood and lymphatic endothelial cells.
Retinoic acid-activated endothelial cells promoted dendritic cell adhesion and transmigration in a ChemR23-dependent manner.
Activated endothelial cells upregulated CCRL2/ACKR5, presenting chemerin to dendritic cells and enhancing transmigration.

Conclusions:

Retinoic acid-activated endothelial cells promote dendritic cell transmigration through endogenous chemerin production and CCRL2 upregulation.
This process involves the activation of dendritic cell β1 integrin affinity and VCAM-1 binding.
The findings highlight a novel mechanism of immune cell trafficking relevant to autoimmune diseases.