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

Objective, To investigate the expression pattern of adhesion molecules invo lved in leukocyte-endothelial cell interactions in giant cell arteritis (GC A), Methods. Immunohistochemical analysis was performed on frozen temporal arte ry sections from 32 patients with biopsy-proven GCA and from 12 control pat ients with other diseases. Adhesion molecules identified were intercellular adhesion molecule 1 (ICAM-1), ICAM-2, ICAM3, vascular cell adhesion molecu le 1 (VCAM-1), platelet endothelial cell adhesion molecule 1 (PECAM-1), E-s electin, 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 inducib le (E-selectin and VCAM-1) endothelial adhesion molecules for leukocytes we re mainly expressed by adventitial microvessels and neovessels within infla mmatory infiltrates. Concurrent analysis of leukocyte receptors indicated a preferential use of VLA-4/VCAM-1 and LFA-1/ICAM-1 at the adventitia and Ma c-1/ICAM-1 at the intima-media junction. The intensity of inducible endothe lial adhesion molecule expression (E-selectin and VCAM-1) correlated with t he 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 i nfiltrates in GCA, The distribution of leukocyte-endothelial cell ligand pa irs suggests a heterogeneity in leukocyte-endothelial cell interactions use d by different functional cell subsets at distinct areas of the temporal ar tery.