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结节病肉芽肿的新发病机制见解。

New pathogenetic insights into the sarcoid granuloma.

作者信息

Agostini C, Adami F, Semenzato G

机构信息

Padua University School of Medicine, Department of Clinical and Experimental Medicine, Clinical Immunology, Italy.

出版信息

Curr Opin Rheumatol. 2000 Jan;12(1):71-6. doi: 10.1097/00002281-200001000-00012.

Abstract

Although the most important enigma of sarcoidosis, ie, its etiology, remains an unsolved problem, the past few years have seen remarkable advances in understanding general immunologic and molecular aspects of the mechanisms leading to granuloma formation in sarcoidosis. It is now clear that during the sarcoid inflammatory process several cytokines are secreted at sites of disease activity; in addition, high affinity receptors for cytokines participating in the granuloma development have been recently identified. This article provides a detailed description of recent data that have clarified cellular interactions governing the dynamics of granuloma formation in sarcoidosis. Together, these new results provide important insights that can refocus efforts at developing immunotherapeutic methods of inhibiting cytokine production at sites of granuloma formation.

摘要

尽管结节病最重要的谜团,即其病因,仍然是一个未解之谜,但在过去几年中,在理解导致结节病肉芽肿形成机制的一般免疫学和分子方面取得了显著进展。现在很清楚,在结节病炎症过程中,几种细胞因子在疾病活动部位分泌;此外,最近还发现了参与肉芽肿形成的细胞因子的高亲和力受体。本文详细描述了最近的数据,这些数据阐明了控制结节病肉芽肿形成动态的细胞相互作用。这些新结果共同提供了重要的见解,可重新聚焦于开发在肉芽肿形成部位抑制细胞因子产生的免疫治疗方法的努力。

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