Pemphigus vulgaris (PV) is an autoimmune blistering disease whose pathogenesis involves both humoral and cell-mediated immune response. Though the pathogenetic role of autoantibodies directed against desmoglein 3 is certain, a number of other factors have been suggested to determine acantholysis in PV. In this study we examined the possible role of CD8+ T cells in the development of acantholysis by a passive transfer of PV autoantibodies using CD8 deficient mice, and we also studied the inflammatory infiltrate of PV skin lesions by immunohistochemical staining. The results of the immunohistochemical staining to study the expression of CD3, CD4, and CD8 in PV skin lesions showed that CD4+ are more expressed than CD8+ in the inflammatory infiltrate of PV lesions, confirming the data of the previous literature. The passive transfer study showed a lower incidence of pemphigus in the group of CD8 deficient mice compared to the control one of wild-type mice. These results suggest that CD8+ T cells may play a role in the pathogenesis of PV, perhaps through the Fas/FasL pathway. 1. Introduction Pemphigus vulgaris (PV) is a life-threatening autoimmune blistering disease mediated by autoantibodies (autoAbs) directed against desmogleins (Dsg) located on the surface of keratinocyte cells (KC). This leads to an intraepithelial loss of adhesion called acantholysis, and clinically it presents with vescicles and blisters [1]. AutoAbs in PV are directed mainly against desmoglein 3 (Dsg 3), a desmosomal glycoprotein situated in the skin predominantly in the suprabasilar epidermal layer, and less frequently against desmoglein 1 [2]. Though the pathogenetic role of antidesmoglein autoAbs is certain, the exact mechanism through which they lead to acantholysis is still incompletely understood. Complement [3], plasminogen-plasmin [4], cytokines [5], cell-mediated immunity, and other autoantibodies such as anticholinergic receptor antibodies have been suggested in determining acantholysis in PV [6]. Studies conducted so far regarding the role of T cells involved mainly CD4+ lymphocytes for their cooperation with B cells and subsequently for the induction and regulation of autoAbs production [7]. The function of CD8+ T cells has not been explored yet, but some authors hypothesize their role in cell-mediated pathogenesis of PV [8]. Other studies suggested a possible role of natural killer (NK) cells [9] as well as Fas and caspase 8 in PV [10]. These molecules’ function in the apoptosis mechanism is well known. In PV these molecules result in a shrinking of keratinocytes that
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