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Antibody-mediated infection and cytotoxic T cells in cosackievirus B3 myocarditis

科萨基病毒 B3 心肌炎中抗体介导的感染和细胞毒性 T 细胞

基本信息

批准号：
03670445
负责人：
KISHIMOTO Chiharu
金额：
$ 1.28万
依托单位：
Toyama Medical & Pharmaceutical University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1991
资助国家：
日本
起止时间：
1991 至 1993
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-03670445/
关键词：
Viral myocarditis Dilated cardiomyopathy Antibody T-lymphocyte Reinfection Superposed infection Coxsackievirus B3

项目摘要

Fc receptor (FcR)-mediated coxsackievirus B3 (CB3) infection in vitro and in vivo was investigated. When P388D1 cells (a murine macrophage-like cell line) were infected with CB3 exposed previously to various concentrations of anti-CB3 rabbit immunoglobulin G (Igg) or its Fab fragment, enhanced infection of CB3 was observed at a subneutralizing concentration of IgG, but not of Fab fragment. In addition, we confirmed the existence of this infectious pathway in vivo. C_3H/He mice with various levels of immunity by preinoculation of amyocarditic CB3 were reinoculated with myocarditic CB3. The severity of myocarditis and myocardial Cb3 titers were markedly enhanced in the mice with a low level of immunity compared to those with high or no immunity. Therefore, the insufficient immunity may not always provide a benign or protective influence. This immunological response facilitates the reinfection possibly inducing chronic active myocarditis.In addition, enterovirus-primed memory T cells would react similarly in vivo to a secondary inoculation with any cardiotropic enterovirus that shares an epitope(s) with the primary challenge virus. Thus, T cell-mediated immune responses to conserved antigenic epitopes among the enteroviruses was involved in the exacerbation of myocardial inflammatory disease during a second enterovirus infection. The secondary infection model may more accurately mirror virus-induced myocarditis in the human population because the majority of adults have exposed t several enteroviruses before induction of disease.

对Fc受体(FCR)介导的柯萨奇病毒B3(CB3)体内外感染进行了研究。用不同浓度的抗CB3兔免疫球蛋白G(Ig G)或其Fab片段感染小鼠巨噬细胞系P388D 1细胞时，在亚中和浓度的Ig G可增强Cb3的感染，而Fab片段则无此作用。此外，我们在体内证实了这种感染途径的存在。将预先接种肌源性CB3的不同免疫水平的C3H/He小鼠再接种心肌CB3。免疫水平低的小鼠与免疫水平高或无免疫水平的小鼠相比，心肌炎的严重程度和心肌CB3滴度显著增加。因此，免疫力不足并不总是提供良性或保护性的影响。这种免疫反应促进了再次感染，可能导致慢性活动性心肌炎。此外，肠道病毒免疫的记忆T细胞在体内对任何与初次挑战病毒具有相同表位(S)的嗜心肠道病毒的二次接种反应相似。因此，T细胞介导的对肠道病毒之间保守抗原表位的免疫反应参与了第二次肠道病毒感染期间心肌炎性疾病的加重。二次感染模型可能更准确地反映人类人群中病毒引起的心肌炎，因为大多数成年人在发病前接触过几种肠道病毒。