CELLULAR STEPS IN THE PATHOGENESIS OF CUTANEOUS NECROTIZING VASCULITIS

Cutaneous necrotizing vasculitis (CNV) have been traditionally divided into ''leukocytoclastic'' and ''lymphomonocytic'' forms, The etiology and the pathogenesis of the two forms are not clear. We studied by im munihistochemistry and electronmicroscopy the infiltrate of 5 cases of leukocytoclastic form and 5 cases of lymphomonocytic form of CNV in t wo phases (early and late), Aim of the study was to evaluate: 1. the i mmunophenotypical characteristics of the infiltrate; 2. the expression of some adhesion molecules receptors; 3. the ultrastructural characte ristic of the infiltrate; 4. the possible sequence of the events, Our results showed, by immunohistochemistry, a rich infiltrate of CD3+, CD 4+, CD1a+ cells in both phases of lympho-monocytic vasculitis and a po or infiltrate of CD4+, CD1a+ and CD36+ cells in the early phase of leu kocytoclastic vasculitis, while the perivascular infiltrate was rich o f these cells in the late phase of this latter form. ICAM-1 and LFA-1 were strongly expressed in lympho-monocytic vasculitis. By electronmic roscopy, most infiltrating cells showing the ultrastructural markers o f immature cells of dendritic lineage were in contact with each other and with lymphocytes and perivascular dendritic macrophages in lymphoc ytic form and in the late phase of leukocytoclastic form. Our results suggest that lymphocytic vasculitis might be related to a cell-mediate d immune reaction and that the leukocytoclastic form of CNV, formerly considered a typical neutrophilic disease, is also maintained by a cel l-mediated immune response to not yet identified endogenous antigens r eleased in the lesional area.