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首页> 外文期刊>Infection and immunity >Trypanosoma cruzi Causes Paralyzing Systemic Necrotizing Vasculitis Driven by Pathogen-Specific Type I Immunity in Mice
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Trypanosoma cruzi Causes Paralyzing Systemic Necrotizing Vasculitis Driven by Pathogen-Specific Type I Immunity in Mice

机译：克氏锥虫引起麻痹性病原体特异性I型免疫驱动的全身性坏死性血管炎

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Infectious agents are often considered potential triggers of chronic inflammatory disease, including autoimmunity; however, direct evidence is usually lacking. Here we show that following control of acute infection of mice with the myotropic Colombiana strain of Trypanosoma cruzi, parasites persisted in tissue at low levels associated with development of systemic necrotizing vasculitis. Lesions occurred in many but not all organs and tissues, with skeletal muscle arteries being the most severely affected, and were associated with myositis, atrophy, paresis/paralysis, and death. Histopathology showed fibrinoid vascular necrosis, rare amastigote nests within skeletal muscle myocytes, and massive leukocyte infiltrates composed mainly of inflammatory monocytes, F4/80+ macrophages, and T. cruzi tetramer-specific CD8+ T lymphocytes capable of producing gamma interferon (IFN-γ) and tumor necrosis factor alpha (TNF-α) but not interleukin-17 (IL-17). T. cruzi-specific IgG was detected in sera from infected mice, but antibody deposits and neutrophilic inflammation were not features of the lesions. Thus, T. cruzi infection of mice may be a specific infectious trigger of paralyzing systemic necrotizing vasculitis most severely affecting skeletal muscle, driven by pathogen-specific type I immune responses.
机译：人们通常认为传染病是慢性炎症疾病的潜在诱因，包括自身免疫。但是，通常缺乏直接的证据。在这里，我们显示在控制了克氏锥虫的肌同性哥伦比亚菌株对小鼠的急性感染的控制后，寄生虫在组织中的持续含量很低，与系统性坏死性血管炎的发展有关。病变发生在许多但并非全部器官和组织中，骨骼肌动脉受的影响最严重，并与肌炎，萎缩，轻瘫/瘫痪和死亡有关。组织病理学检查显示纤维蛋白样血管坏死，骨骼肌肌细胞内罕见的鞭毛体巢和大量浸润性白细胞浸润，主要由炎性单核细胞，F4 / 80 +巨噬细胞以及克鲁斯四聚体特异性CD8 + T淋巴细胞产生，可​​产生γ-干扰素（IFN-γ）。和肿瘤坏死因子α（TNF-α），但白介素17（IL-17）没有。在感染小鼠的血清中检测到了克鲁维弧菌特异性IgG，但抗体沉积和嗜中性粒细胞炎症并不是病变的特征。因此，小鼠的克氏锥虫感染可能是由病原体特异性I型免疫反应驱动的，最严重影响骨骼肌的麻痹全身性坏死性血管炎的特定感染触发物。

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