A Possible Role for CD8+ T Lymphocytes in the Cell-Mediated Pathogenesis of Pemphigus Vulgaris

被引:18
|
作者
Giurdanella, Federica [1 ]
Fania, Luca [1 ]
Gnarra, Maria [1 ]
Toto, Paola [2 ]
Di Rollo, Daniela [3 ]
Sauder, Daniel N. [4 ,5 ]
Feliciani, Claudio [1 ]
机构
[1] Univ Cattolica Sacro Cuore, Policlin A Gemelli Hosp, Dept Dermatol, I-00168 Rome, Italy
[2] Univ G dAnnunzio, Dept Dermatol, I-66013 Chieti, Italy
[3] Univ G dAnnunzio, Dept Med & Aging Sci, I-66013 Chieti, Italy
[4] Princeton Univ Hosp, Dept Dermatol, Princeton, NJ 08540 USA
[5] Univ Ottawa, Fac Med, Ottawa, ON K1H 8M5, Canada
关键词
D O I
10.1155/2013/764290
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
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