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致癌性炎症与自身免疫性疾病。

Oncogenic inflammation and autoimmune disease.

作者信息

Eisenlohr Laurence C, Rothstein Jay L

机构信息

Departments of Microbiology/Immunology and Otolaryngology-HNS, Kimmel Cancer Center, Thomas Jefferson University, 233 South 10th Street, Philadelphia, PA 19107, USA.

出版信息

Autoimmun Rev. 2006 Dec;6(2):107-14. doi: 10.1016/j.autrev.2006.04.002. Epub 2006 May 22.

Abstract

Many models exist to explain the induction and perpetuation of autoimmune diseases. Despite their validation in a variety of animal models, the basis for autoimmune disease in humans remains unknown. Here, we propose that an important aspect of autoimmune disease is the active participation of the target organ due to endogenously produced co-stimulatory factors that cause prolonged antigen presentation and lymphocyte activation. Evidence suggests that a major source of such endogenous signaling comes from newly transformed cells within the target organ that produce pro-inflammatory factors.

摘要

存在多种模型来解释自身免疫性疾病的诱导和持续存在。尽管它们在多种动物模型中得到了验证,但人类自身免疫性疾病的发病机制仍然未知。在此,我们提出自身免疫性疾病的一个重要方面是靶器官的主动参与,这是由于内源性产生的共刺激因子导致抗原呈递延长和淋巴细胞活化。有证据表明,这种内源性信号的一个主要来源是靶器官内新转化的细胞,这些细胞会产生促炎因子。

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