摘要
Background: The link between the lupus band and pathogenesis remains controver sial, because immunoglobulins and complement components, including the membrane attack complex, can be found in both lesional and non-lesional skin of patients with systemic lupus erythematosus (SLE). The expression of proteins that regula te complement has not been previously investigated in the skin of patients with SLE. Aim: The aim of this study is to compare the expression of protectin (CD59) , which demonstrates the activation of the classical pathway of complement, in n on-lesional skin obtained from patients with SLE with its expression in normal skin. This may help us explain the link between the lupus band and pathogenesis of cutaneous lupus erythematosus. Methods: An indirect immunofluorescence techni que was performed in order to provide unequivocal evidence for the activation of complement via the classical pathway and to compare the expression of CD59 in n on-lesional skin from patients with SLE with normal skin samples obtained from healthy people. Results: The activation of the classical pathway of complement w as demonstrated in non-lesional skin inmore than 90%of SLE patients investigat ed in this study. Staining intensity of the complement regulatory proteinCD59was markedly increased in themajority of non-lesional skin samples obtained from p atientswith SLE, compared to that from normals. Conclusions: CD59 is overexpress ed in non-lesional skin in which complement activation has occurred. It seems l ikely that an increased and continuous CD59 expression may be important for main taining the integrity of the skin BMZ during inflammatory responses involving co mplement activation in SLE skin.
Background: The link between the lupus band and pathogenesis remains controver sial, because immunoglobulins and complement components, including the membrane attack complex, can be found in both lesional and non-lesional skin of patients with systemic lupus erythematosus (SLE). The expression of proteins that regula te complement has not been previously investigated in the skin of patients with SLE. Aim: The aim of this study is to compare the expression of protectin (CD59) , which demonstrates the activation of the classical pathway of complement, in n on-lesional skin obtained from patients with SLE with its expression in normal skin. This may help us explain the link between the lupus band and pathogenesis of cutaneous lupus erythematosus. Methods: An indirect immunofluorescence techni que was performed in order to provide unequivocal evidence for the activation of complement via the classical pathway and to compare the expression of CD59 in n on-lesional skin from patients with SLE with normal skin samples obtained from healthy people. Results: The activation of the classical pathway of complement w as demonstrated in non-lesional skin inmore than 90%of SLE patients investigat ed in this study. Staining intensity of the complement regulatory proteinCD59was markedly increased in themajority of non-lesional skin samples obtained from p atientswith SLE, compared to that from normals. Conclusions: CD59 is overexpress ed in non-lesional skin in which complement activation has occurred. It seems l ikely that an increased and continuous CD59 expression may be important for main taining the integrity of the skin BMZ during inflammatory responses involving co mplement activation in SLE skin.
