On the relationship between viral infection and autoimmunity
On the relationship between viral infection and autoimmunity
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DOI：
10.1006/jaut.2000.0480
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发表时间：
2001-05-01
影响因子：
12.8
通讯作者：
Cantor, H
中科院分区：
文献类型：
--
作者：
Panoutsakopoulou, V;Cantor, H
器官特异性自身免疫被认为是由于丧失对自身抗原的耐受性。然而，仅仅存在潜在的自身反应性T细胞通常不足以诱发自身免疫性疾病。人们对诸如微生物病原体等环境因素可能参与触发这些细胞和引发疾病的可能性给予了相当大的关注。事实上，病毒感染常常先于糖尿病的发病[1-3]和多发性硬化症的复发[1-3]。小鼠微生物感染可诱发糖尿病[3]、脱髓鞘病[5-7]、间质角膜炎[8-10]和心肌炎[11]。虽然感染和疾病之间联系的分子基础尚不完全清楚，但病原体诱导的炎症反应被认为起着核心作用。
Organ-specific autoimmunity is thought to result from loss of tolerance to self-antigens. However, the mere presence of potentially autoreactive T cells is generally not sufficient to induce autoimmune disease. Considerable attention has been given to the possibility that environmental factors such as microbial pathogens may be involved in triggering these cells and inciting disease. Indeed, viral infection often precedes the onset of diabetes [1–3] and relapses of multiple sclerosis [4]. Murine microbial infections can precipitate diabetes [3], demyelinating disease [5–7], stromal keratitis [8–10] and myocarditis [11]. Although the molecular basis of the link between infection and disease is not fully understood, pathogen-induced inflammatory responses are thought to play a central role.