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神经免疫性疾病的发病机制。实验模型。

Pathogenesis of neuroimmunologic diseases. Experimental models.

作者信息

Constantinescu C S, Hilliard B, Fujioka T, Bhopale M K, Calida D, Rostami A M

机构信息

Department of Neurology, University of Pennsylvania Medical Center, Philadelphia 19104, USA.

出版信息

Immunol Res. 1998;17(1-2):217-27. doi: 10.1007/BF02786446.

DOI:10.1007/BF02786446
PMID:9479583
Abstract

Animal models of autoimmune diseases have greatly improved our current understanding of the pathogenesis of human autoimmunity and have provided the potential for therapies based on manipulation of the immune system. In our laboratory, we have investigated the immunopathogenesis of autoimmune diseases of the nervous system and muscle. We have developed immune-based approaches for the suppression of experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis (MS), and experimental autoimmune neuritis (EAN), a model for the Guillain-Barré syndrome (GBS). These approaches included induction of peripheral tolerance, immunotoxin targeting of activated T cells, and cytokine manipulations. In addition, we identified the antigen and characterized immunopathologically an autoimmune inflammatory disease of skeletal muscle, experimental autoimmune myositis (EAM), a model for the human inflammatory muscle disease polymyositis.

摘要

自身免疫性疾病的动物模型极大地增进了我们目前对人类自身免疫发病机制的理解,并为基于免疫系统调控的治疗方法提供了可能性。在我们实验室,我们研究了神经系统和肌肉自身免疫性疾病的免疫发病机制。我们已开发出基于免疫的方法来抑制实验性自身免疫性脑脊髓炎(EAE,一种多发性硬化症(MS)模型)和实验性自身免疫性神经炎(EAN,一种吉兰 - 巴雷综合征(GBS)模型)。这些方法包括诱导外周耐受、针对活化T细胞的免疫毒素靶向以及细胞因子调控。此外,我们鉴定出了抗原,并对骨骼肌的一种自身免疫性炎症疾病——实验性自身免疫性肌炎(EAM,一种人类炎症性肌肉疾病多发性肌炎的模型)进行了免疫病理学特征分析。

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