摘要
Background: Current evidence suggests that lichen planus is a T-cell-mediated autoimmune disease in which cytotoxic mechanisms have been poorly investigated. Objectives: We investigated the expression of perforin in subpopulations of peripheral blood lymphocytes(PBL) in exacerbation and remission phases of the disease as well as in skin lesions. Methods: We performed a simultaneous detection of perforin (intracellular molecule) and cell surface antigens on PBL by flow cytometry, and skin lesions were investigated by immunohistochemistry. Results: The most interesting finding was a significant increase of perforin expression in cytotoxic T lymphocytes (CD3+perforin+cells) in the exacerbation phase of disease(P < 0.05), which was mostly located in the CD8+subpopulation (CD8+perforin+) (P < 0.01). Using immunohistochemistry we confirmed the infiltration of T lymphocytes in skin lesions, especially of CD4+and CD8+phenotypes, compared with uninvolved (P < 0.05) and healthy skin (P < 0.01). The expression of perforin was also significantly higher in lesional skin compared with nonlesional and healthy skin (P < 0.05). Conclusions: Our results clearly show the upregulation of perforin expression in peripheral blood as well as in lesions of patients with lichen planus and therefore suggest an important role for perforin in this autoimmune disease.
Background: Current evidence suggests that lichen planus is a T-cell-mediated autoimmune disease in which cytotoxic mechanisms have been poorly investigated. Objectives: We investigated the expression of perforin in subpopulations of peripheral blood lymphocytes(PBL) in exacerbation and remission phases of the disease as well as in skin lesions. Methods: We performed a simultaneous detection of perforin (intracellular molecule) and cell surface antigens on PBL by flow cytometry, and skin lesions were investigated by immunohistochemistry. Results: The most interesting finding was a significant increase of perforin expression in cytotoxic T lymphocytes (CD3+perforin+cells) in the exacerbation phase of disease(P < 0.05), which was mostly located in the CD8+subpopulation (CD8+perforin+) (P < 0.01). Using immunohistochemistry we confirmed the infiltration of T lymphocytes in skin lesions, especially of CD4+and CD8+phenotypes, compared with uninvolved (P < 0.05) and healthy skin (P < 0.01). The expression of perforin was also significantly higher in lesional skin compared with nonlesional and healthy skin (P < 0.05). Conclusions: Our results clearly show the upregulation of perforin expression in peripheral blood as well as in lesions of patients with lichen planus and therefore suggest an important role for perforin in this autoimmune disease.
