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(Circulation Research. 2000;86:1190.)
© 2000 American Heart Association, Inc.

Editorials

Lymphocyte Trafficking Mediated by Vascular Adhesion Protein-1

Implications for Immune Targeting and Cardiovascular Disease

J. Steven Alexander, D. Neil Granger

From the Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, La.

Correspondence to J. Steven Alexander, PhD, Department of Molecular and Cellular Physiology, LSU Health Sciences Center, 1501 Kings Highway, Shreveport, LA 71130-3932. E-mail jalexa@lsumc.edu

Key Words: lymphocytes • cardiovascular disease • vascular adhesion protein-1

	Introduction

 
The trafficking, extravasation, and retention of lymphocytes within certain tissues (eg, lymph nodes) seem to be mediated by several classes of specialized adhesion glycoproteins that are expressed on the surface of unique endothelial cells (high endothelial venules [HEVs]) that exist in both the blood and lymph microvessels.^{1 2} The binding of these endothelial cell adhesion molecules to their corresponding ligands on lymphocytes (L-selectin, ₄ß₇, ₄ß₁, leukocyte function–associated antigen-1 [LFA-1], and CLA-1) tightly controls the kinetics and magnitude of lymphocyte margination, rolling, adhesion, and extravasation, thereby allowing these leukocytes to fulfill their immune surveillance functions and, in some tissues, mature into fully differentiated cells. During inflammation, the recruitment and retention of lymphocytes in affected tissues occur at an accelerated rate, because locally released mediators (eg, cytokines, chemokines, and oxidants) increase the expression of relevant adhesion molecules on both the endothelial cells and leukocytes.

Although much progress has been made in our understanding of the molecular determinants of lymphocyte–endothelial cell adhesion in the blood circulation, the identification and characterization of the glycoproteins that mediate this cell-cell adhesive interaction has tended to lag behind equivalent efforts made for neutrophil–endothelial cell adhesion.^{3 4 5} Nonetheless, the efforts to discover and characterize adhesive determinants on both leukocyte populations have led to the revelation that lymphocytes and neutrophils share several glycoproteins, including ß₂-integrins (CD11/CD18), and L-selectin. As a consequence of these observations, the initial models that were proposed to explain the coordinated recruitment of leukocytes to sites of inflammation assumed that neutrophils and lymphocytes followed the . . . [Full Text of this Article]