Comparison of cell adhesion molecule expression in cutaneous leucocytoclastic and lymphocytic vasculitis.

摘要

AIMS--To compare the expression of the cell adhesion molecules intercellular adhesion molecule-1 (ICAM-1), ELAM-1 (E-selectin), and vascular cell adhesion molecule-1 (VCAM-1) in cutaneous leucocytoclastic and lymphocytic vasculitis. METHODS--Immunohistochemical analysis was performed on early lesional skin biopsy specimens of leucocytoclastic vasculitis (n = 14), lymphocytic vasculitis (n = 10), non-lesional skin (n = 12), and normal skin (n = 5). A standard immunoperoxidase technique was used to detect expression of ICAM-1, E-selectin, VCAM-1, and the cell markers CD11a, CD11b, CD11c, von Willebrand factor, CD3, CD68, and neutrophil elastase (NP57). RESULTS--Basal keratinocyte intercellular adhesion molecule-1 was expressed in eight (80%) cases of lymphocytic and in only one (7%) case of leucocytoclastic vasculitis, and not in non-lesional skin or control biopsy specimens from normal subjects. E-selectin was expressed on vascular endothelium in eight (57%) cases of leucocytoclastic and in seven (70%) cases of lymphocytic vasculitis. Endothelial vascular cell adhesion molecule-1 expression was seen in three (21%) biopsy specimens of leucocytoclastic and five (50%) of lymphocytic vasculitis. There were increased numbers of cells in the dermal infiltrate stained for NP57, CD11b, and CD11c in leucocytoclastic compared with lymphocytic vasculitis (p < 0.001, p = 0.013, p = 0.009, respectively); immunoreactive positive cells for CD3 and CD11a were increased in lymphocytic compared with leucocytoclastic vasculitis (p < 0.001, p = 0.011, respectively). CONCLUSIONS--These observations indicate that upregulation of adhesion molecule expression occurs in both leucocytoclastic and lymphocytic vasculitis. The different patterns of adhesion molecule expression in the two groups of vasculitis may reflect differences in the local release of cytokines. In particular, detection of intercellular adhesion molecule-1 expression by keratinocytes in lymphocytic vasculitis is consistent with an active role for mediators derived from T lymphocytes in the pathogenesis of the lesion.