Ytterberg S R, Mahowald M L, Messner R P
J Clin Invest. 1987 Aug;80(2):499-506. doi: 10.1172/JCI113098.
Chronic inflammatory myositis similar to human polymyositis occurs in mice after infection with a strain of Coxsackievirus B 1 (CVB 1). To investigate the role of T cells in the pathogenesis of this disorder, we compared disease expression in T cell-deficient athymic nude (nu/nu) mice and heterozygotes (nu/+) with normal T cell function. Acute infectious myositis occurred in nu/nu and nu/+ mice. Chronic (greater than 21 d postinfection) weakness and myositis, however, developed only in nu/+. Resistance to disease in nu/nu mice was not explained by insusceptibility to infection; the amount of virus lethal for 50% of mice and virus replication were comparable in both groups. Additionally, anti-CVB 1 antibody production was similar in both groups. Reconstitution of infected nu/nu mice with spleen cells from normal mice resulted in disease. These results demonstrate that chronic weakness after infection with this virus is not simply a sequela of acute myonecrosis and suggest that T cells play a pivotal role in the pathogenesis of chronic myositis.
感染柯萨奇病毒B1(CVB1)毒株后,小鼠会出现类似于人类多发性肌炎的慢性炎症性肌炎。为了研究T细胞在这种疾病发病机制中的作用,我们比较了T细胞缺陷的无胸腺裸鼠(nu/nu)和具有正常T细胞功能的杂合子(nu/+)小鼠的疾病表现。急性感染性肌炎在nu/nu和nu/+小鼠中均有发生。然而,慢性(感染后超过21天)肌无力和肌炎仅在nu/+小鼠中出现。nu/nu小鼠对疾病的抵抗力并非由于对感染不敏感所致;两组中对50%小鼠致死的病毒量和病毒复制情况相当。此外,两组中抗CVB1抗体的产生情况相似。用正常小鼠的脾细胞重建感染的nu/nu小鼠会导致疾病发生。这些结果表明,感染该病毒后的慢性肌无力并非仅仅是急性肌坏死的后遗症,提示T细胞在慢性肌炎的发病机制中起关键作用。