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柯萨奇病毒B3型诱导Balb/C小鼠发生心肌炎的细胞免疫机制

Cellular immune mechanisms in Coxsackievirus group B, type 3 induced myocarditis in Balb/C mice.

作者信息

Huber S A, Job L P

出版信息

Adv Exp Med Biol. 1983;161:491-508. doi: 10.1007/978-1-4684-4472-8_29.

Abstract

Coxsackie B viruses are a common cause of viral myocarditis in humans. A murine model of the human disease has been developed using Coxsackievirus group B, type 3 and inbred Balb/c mice. Infection of T lymphocyte deficient mice does not result in significant myocarditis indicating the importance of T cells in this disease. The virus can be isolated from the hearts of T cell deficient and normal mice in equal concentrations. Virus elimination presumably is mediated by virus specific neutralizing antibody induced in both groups. T lymphocytes, natural killer cells and macrophage obtained from normal virus infected mice are all capable of lysing myofibers in vitro. Maximum lysis is obtained with the cytolytic T cells. When these cell populations or Coxsackievirus immune antibody were adoptively transferred into T lymphocyte deficient animals infected with the virus, only animals given T cells developed significant myocarditis.

摘要

柯萨奇B病毒是人类病毒性心肌炎的常见病因。利用B组3型柯萨奇病毒和近交系Balb/c小鼠建立了人类疾病的小鼠模型。感染T淋巴细胞缺陷小鼠不会导致显著的心肌炎,这表明T细胞在这种疾病中具有重要作用。病毒可从T细胞缺陷小鼠和正常小鼠的心脏中以相同浓度分离出来。病毒清除可能是由两组中诱导产生的病毒特异性中和抗体介导的。从正常感染病毒的小鼠中获得的T淋巴细胞、自然杀伤细胞和巨噬细胞在体外均能裂解肌纤维。细胞毒性T细胞可实现最大程度的裂解。当将这些细胞群体或柯萨奇病毒免疫抗体过继转移到感染该病毒的T淋巴细胞缺陷动物中时,只有接受T细胞的动物出现了显著的心肌炎。

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