利用病毒融合蛋白单克隆抗体改善裸鼠仙台病毒性肺炎。

P Carthew, J Riley, D Dinsdale
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引用次数: 0

摘要

已知副流感I型(仙台病毒)的病理作用是支气管肺炎,在免疫缺陷胸腺(裸)小鼠中变为慢性肺炎。这种慢性肺炎的严重程度可以通过给裸鼠提供体液单克隆抗体来显著改变,这些抗体可以中和病毒的融合蛋白,并直接针对病毒的融合蛋白。肺泡炎是病理的重要组成部分,由于肺泡中存在的病毒感染的肺泡巨噬细胞数量减少(大于90%)而受到抑制。这清楚地确定了感染的肺泡巨噬细胞是i型副流感病毒引起的肺泡炎发病机制中的主要效应细胞。本文讨论了使用病毒中和单克隆抗体治疗病毒性肺炎的意义,这种单克隆抗体几乎没有免疫调节毒性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Amelioration of established Sendai viral pneumonia in the nude mouse using a monoclonal antibody to the virus fusion protein.

The pathological effect of parainfluenza type I (Sendai virus) is known to be a bronchopneumonia, which becomes a chronic pneumonia in the immunodeficient athymic (nude) mouse. The severity of this established chronic pneumonia can be dramatically altered by providing the nude mouse with humoral monoclonal antibodies which are neutralizing, and are directed against the fusion protein, of the virus. The alveolitis, which is a significant part of the pathology, is suppressed due to a reduction (greater than 90%) in the number of virus-infected alveolar macrophages present in the alveoli. This clearly identifies the infected alveolar macrophage as the primary effector cell in the pathogenesis of alveolitis caused by parainfluenza virus type I. The implications of using virus-neutralizing monoclonal antibodies, which have little immunomodulatory toxicity, in the treatment of viral pneumonias are discussed.

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