BACKGROUND:Pemphigus is an autoimmune disease characterized by intraepidermal blisters induced by pemphigus IgG. In addition to autoantibodies, molecular mechanisms involved in acantholysis remain largely unknown. For this reason, we address a possible role of the inflammatory cytokines IL-6 and TNFalpha in pemphigus lesions. METHODS:Sixteen biopsies from patients with different types of pemphigus were studied by in situ hybridization using DNA fluorescent probes for IL-6 and TNFalpha mRNA. RESULTS:Fifty-six percent of lesional biopsies exhibited cytokine gene expression, which was poorly expressed in noninvolved skin. Deposits of TNFalpha and IL-6 were products of in situ transcription at the epidermal level. CONCLUSIONS:Inflammatory cytokine expression around the blister could play a mediator role in pemphigus lesions by increasing epithelial damage.

译文

背景:天疱疮是一种自身免疫性疾病,以天疱疮IgG诱导的表皮内水泡为特征。除自身抗体外,棘皮松解所涉及的分子机制仍然未知。因此,我们探讨了炎性细胞因子IL-6和TNFalpha在天疱疮病变中的可能作用。
方法:采用DNA荧光探针对IL-6和TNFαmRNA进行原位杂交,对16例不同类型天疱疮患者进行活检。
结果:56%的病灶活检组织显示了细胞因子基因的表达,在不累及的皮肤中表达较差。 TNFα和IL-6的沉积物是表皮水平的原位转录产物。
结论:水疱周围炎性细胞因子的表达可能通过增加上皮损伤而在天疱疮病变中起介导作用。

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