Chosen selectins and integrins in systemic sclerosis skin lesions

Systemic scleroderma is a progressive condition characterized by inflammation and fibrosis of the skin and internal organs. Autoimmune mechanisms that operate in patients with SSc, as well as the presence of activated fibroblasts, endothelial cells and lymphocytes, including T cells, have been documented. Several studies have suggested that overexpression of selected adhesion molecules contributes to the homing of activated lymphocytes to the skin of patients with early scleroderma. The cell-extracellular matrix (ECM) interactions are mediated through distinct receptors on the cell surface, mainly integrins. Integrins are heterodimeric receptors for cell surface counterreceptors, as well as ECM proteins. Literature data about selectins and integrins in scleroderma are controversial. The aim of our study was to assess the expression of selected adhesion molecules – selectins and integrins – in systemic sclerosis skin biopsies by immunohistochemistry method. Selected adhesion molecules showed different expression: L-selectin was detected in the epithelium and skin leukocytes in samples of early scleroderma skin with infiltration, the moderate expression of E-selectin in endothelial cells, expression of selected integrins in basal keratinocytes in scleroderma tissue specimens and focally in the other layers of the epidermis. Neutrophils in perivascular infiltrations and basal keratinocytes stained positive for bβ and β3 integrins. Expression of β4 integrin was detected in basal keratinocytes and was of regular and linear type. In all samples obtained from healthy volunteers expression of the examined molecules was weak, detected only in single basal keratinocytes and endothelium cells. Our results suggest that integrins and selectins may play an important role in the pathogenesis of early scleroderma skin pathology. Impaired expression of selectins and integrins, stimulated by immune mechanisms, may be responsible for formation of skin lesions.