Abstract
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.
Highlights
Pemphigus vulgaris (PV) is a life-threatening autoimmune blistering disease mediated by autoantibodies directed against desmogleins (Dsg) located on the surface of keratinocyte cells (KC)
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 studied the inflammatory infiltrate of PV skin lesions by immunohistochemical staining
These results suggest that CD8+ T cells may play a role in the pathogenesis of PV, perhaps through the Fas/Fas ligand (FasL) pathway
Summary
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]. 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 this study we sought to evaluate the role of CD8+ cells performing a passive transfer of PV autoAbs using CD8 deficient mice (CD8−/−) The results of these studies suggest a role for CD8 in the pathogenesis of PV
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