CELL ADHESION MOLECULES IN THE DEVELOPMENT OF INFLAMMATORY INFILTRATES IN GIANT CELL ARTERITIS: Inflammation-Induced Angiogenesis as the Preferential Site of Leukocyte–Endothelial Cell Interactions

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Objective.To investigate the expression pattern of adhesion molecules involved in leukocyte–endothelial cell interactions in giant cell arteritis (GCA).Methods.Immunohistochemical analysis was performed on frozen temporal artery sections from 32 patients with biopsy-proven GCA and from 12 control patients with other diseases. Adhesion molecules identified were intercellular adhesion molecule 1 (ICAM-1), ICAM-2, ICAM-3, vascular cell adhesion molecule 1 (VCAM-1), platelet endothelial cell adhesion molecule 1 (PECAM-1), E-selectin, P-selectin, L-selectin, lymphocyte function–associated antigen 1 (LFA-1), very late activation antigen 4 (VLA-4), Mac-1 (CD18/CD11b), and gp 150,95 (CD18/CD11c). Clinical and biochemical parameters of inflammation in the patients, as well as the duration of previous corticosteroid treatment, were prospectively recorded.Results.Constitutive (PECAM-1, ICAM-1, ICAM-2, and P-selectin) and inducible (E-selectin and VCAM-1) endothelial adhesion molecules for leukocytes were mainly expressed by adventitial microvessels and neovessels within inflammatory infiltrates. Concurrent analysis of leukocyte receptors indicated a preferential use of VLA-4/VCAM-1 and LFA-1/ICAM-1 at the adventitia and Mac-1/ICAM-1 at the intima–media junction. The intensity of inducible endothelial adhesion molecule expression (E-selectin and VCAM-1) correlated with the intensity of the systemic inflammatory response. Previous corticosteroid treatment reduced, but did not completely abrogate, the expression of the inducible endothelial adhesion molecules E-selectin and VCAM-1.Conclusion.Inflammation-induced angiogenesis is the main site of leukocyte–endothelial cell interactions leading to the development of inflammatory infiltrates in GCA. The distribution of leukocyte–endothelial cell ligand pairs suggests a heterogeneity in leukocyte–endothelial cell interactions used by different functional cell subsets at distinct areas of the temporal artery.

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