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角质形成细胞中组胺非依赖性瘙痒介质的异常表达可能与结节性痒疹的发病机制有关。

Aberrant Expression of Histamine-independent Pruritogenic Mediators in Keratinocytes may be Involved in the Pathogenesis of Prurigo Nodularis.

机构信息

Department of Dermatology, Peking University First Hospital, Beijing 100034, China.

出版信息

Acta Derm Venereol. 2019 May 1;99(6):579-586. doi: 10.2340/00015555-3150.

DOI:10.2340/00015555-3150
PMID:30809683
Abstract

Prurigo nodularis is a highly pruritic and hyperplastic chronic dermatosis with unknown pathogenesis. Many pruritogenic mediators, including nerve growth factor, interleukin (IL)-31, thymic stromal lymphopoietin, and endothelin-1, are implicated in chronic itch and inflammation. This study investigated the mRNA levels and immunoreactivity of the nerve growth factor, IL-31, thymic stromal lymphopoietin, and endothelin axes in both lesional and perilesional skin in prurigo nodularis by using quantitative real-time PCR and immunohistochemistry studies. The nerve growth factor high-affinity receptor tyrosine kinase receptor A was upregulated while the low affinity receptor p75 neurotrophin receptor was downregulated in prurigo nodularis lesions. Downregulated expression of IL-31/IL-31 receptor A and endothelin-3/endothelin receptor B and upregulation of thymic stromal lymphopoietin receptor were found in prurigo nodularis lesions. Aberrant expression of nerve growth factor, IL-31, thymic stromal lymphopoietin and endothelin axes was found in prurigo nodularis lesions, especially in the epidermis, indicating the importance of keratinocytes in prurigo nodularis pathogenesis.

摘要

结节性痒疹是一种高度瘙痒和增生性的慢性皮肤病,其发病机制尚不清楚。许多瘙痒诱发介质,包括神经生长因子、白细胞介素 (IL)-31、胸腺基质淋巴细胞生成素和内皮素-1,与慢性瘙痒和炎症有关。本研究通过定量实时 PCR 和免疫组织化学研究,探讨了神经生长因子、IL-31、胸腺基质淋巴细胞生成素和内皮素轴在结节性痒疹皮损和皮损周围皮肤中的 mRNA 水平和免疫反应性。在结节性痒疹皮损中,神经生长因子高亲和力受体酪氨酸激酶受体 A 上调,而低亲和力受体 p75 神经营养因子受体下调。在结节性痒疹皮损中发现 IL-31/IL-31 受体 A 和内皮素-3/内皮素受体 B 的表达下调,以及胸腺基质淋巴细胞生成素受体的上调。在结节性痒疹皮损中发现神经生长因子、IL-31、胸腺基质淋巴细胞生成素和内皮素轴的异常表达,尤其是在表皮中,表明角质形成细胞在结节性痒疹发病机制中的重要性。

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