CD137 is expressed on blood vessel walls at sites of inflammation and enhances monocyte migratory activity

Drenkard, Daniela and Becke, Florian M. and Langstein, Joachim and Spruss, Thilo and Kunz-Schughart, Leoni A. and Tan, Teng Ee and Lim, Yaw Chyn and Schwarz, Herbert (2007) CD137 is expressed on blood vessel walls at sites of inflammation and enhances monocyte migratory activity. FASEB JOURNAL, 21 (2). pp. 456-463. ISSN 0892-6638, 1530-6860

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Abstract

The cytokine receptor CD137 is a member of the TNF receptor family and a potent T cell costimulatory molecule. Its ligand is expressed on antigen presenting cells as a transmembrane protein and it too can deliver signals into the cells it is expressed on (reverse signaling). In monocytes, immobilized CD137 protein induces activation, prolongation of survival and proliferation. Here we show that recombinant immobilized CD137 protein enhances migration of monocytes in vitro. Further, CD137 expression on spheroids leads to a significantly enhanced infiltration by monocytes. The migration-inducing activity of CD137 could be confirmed in vivo. Matrigel, which was coated with recombinant CD137 protein and was inserted into the flanks of mice attracted large numbers of monocytes and was heavily infiltrated by these cells. In vivo, expression of CD137 by blood vessel walls at sites of inflammation was detectable by immunohistochemistry. CD 137 expression is inducible by proinflammatory cytokines in endothelial cells, suggesting that a physiological function of CD 137 may be the facilitation of monocyte extravasation in inflammatory tissues.

Item Type: Article
Uncontrolled Keywords: FACTOR-RECEPTOR FAMILY; DENDRITIC CELLS; 4-1BB LIGAND; LYMPHOCYTE-ACTIVATION; IN-VIVO; PROLIFERATION; SELECTINS; SURVIVAL; ADHESION; MEMBER; extravasation; vascular biology
Subjects: 600 Technology > 610 Medical sciences Medicine
Divisions: Medicine > Lehrstuhl für Pathologie
Depositing User: Dr. Gernot Deinzer
Date Deposited: 22 Dec 2020 11:57
Last Modified: 22 Dec 2020 11:58
URI: https://pred.uni-regensburg.de/id/eprint/33225

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