Lichenoid dermatitis in paraneoplastic pemphigus -: A pathogenic trigger of epitope spreading?
Lichenoid dermatitis in paraneoplastic pemphigus -: A pathogenic trigger of epitope spreading?
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DOI：
10.1001/archderm.136.5.652
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发表时间：
2000-05-01
影响因子：
--
通讯作者：
Stevens, SR
中科院分区：
文献类型：
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作者：
Bowen, GM;Peters, NT;Stevens, SR
背景：在某些病例中，已观察到扁平苔藓是一种副肿瘤性疾病，有时与副肿瘤性天疱疮相关，这是一种以斑蛋白、桥粒芯糖蛋白 3 和 1 以及尚未表征的 170-kd 抗原为特征的自身抗体的疾病。表位扩散描述了这样一种现象：随着时间的推移，潜在的慢性炎症会导致自身蛋白上新表位的顺序识别。观察结果：诊断为副肿瘤性天疱疮的 6 名患者中有 5 名伴有扁平苔藓的临床和组织学特征。 1 例患者的大鼠膀胱初始间接免疫荧光结果为阴性，免疫沉淀仅鉴定出 5 种抗原中的 2 种。经过一年的疾病恶化，反复测试证实存在针对所有 6 种相关抗原的抗体，支持我们的假设，即副肿瘤性天疱疮可能发生表位扩散。结论：苔藓样皮疹可能导致副肿瘤性天疱疮的早期进化阶段。真皮表皮连接处的细胞介导的自身免疫可能促进自身抗原的暴露以及随后和进行性体液自身免疫的发展。因此，副肿瘤性天疱疮可能在人类体液介导的自身免疫性疾病中表现出表位扩散。
Background: In select cases, lichen planus has been observed to be a paraneoplastic condition sometimes associated with paraneoplastic pemphigus, a disease featuring autoantibodies directed against plakin proteins, desmogleins 3 and 1, and a still uncharacterized 170-kd antigen. Epitope spreading describes the phenomenon where underlying chronic inflammation leads to the sequential recognition of new epitopes on self-proteins over time.Observations: Five of 6 patients diagnosed as having paraneoplastic pemphigus had concomitant clinical and histological features of lichen planus. In 1 patient, re suits of the initial indirect immunofluorescence on rat bladder were negative and only 2 of the 5 antigens were identified by immunoprecipitation. After 1 year of worsening disease, repeated testing confirmed the presence of antibodies directed against all 6 of the implicated antigens, supportive of our hypothesis that epitope spreading may occur in paraneoplastic pemphigus.Conclusions: Lichenoid eruptions may predispose to an early evolutionary stage of paraneoplastic pemphigus. Cell-mediated autoimmunity at the dermoepidermal junction may promote the exposure of self-antigens and the development of subsequent and progressive humoral autoimmunity. As such, paraneoplastic pemphigus may demonstrate epitope spreading in a human, humoral-mediated autoimmune disease.