银屑病
菱形
发病机制
下调和上调
免疫组织化学
医学
病理
免疫学
癌症研究
生物
信号转导
细胞生物学
生物化学
基因
罗亚
作者
Zhen F. Tian,Wenghong Wong,Qiong Wu,Jiaqing Zhou,Kexiang Yan,Jia Chen,Zhenghua Zhang
出处
期刊:Applied Immunohistochemistry & Molecular Morphology
日期:2021-09-16
卷期号:30 (2): 119-125
被引量:5
标识
DOI:10.1097/pai.0000000000000977
摘要
Psoriasis is a chronic, immune-mediated inflammatory disease which pathogenesis is closely linked to γδ T cells. Recently, a critical role for butyrophilin 3A1 (BTN3A1) in mediating the activation of Vγ9Vδ2 T cells, which are reported to redistribute from blood to the perturbed skin lesions in psoriasis, has been proposed. Additional molecular partners, including RhoB and periplakin, have also been speculated to interact with BTN3A1 in modulating Vγ9Vδ2 T-cell activation. Immunohistochemical staining was performed to examine the expressions of BTN3A1, RhoB, and the plakin family members, including periplakin, epiplakin, and envoplakin in the psoriasis vulgaris lesions as compared with the normal control. The expressions of BTN3A1 and RhoB were found significantly upregulated in the psoriatic lesions. Besides, a downregulation of periplakin and an upregulation of epiplakin were noticed in the psoriasis vulgaris lesions. Our data suggest that BTN3A1 and RhoB might participate in the pathogenesis of psoriasis through Vγ9Vδ2 T-cell responses. In addition, a potential involvement of the plakin protein family, especially periplakin and epiplakin, in psoriasis pathology was proposed.
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