Estrin M, Smith C, Huber S
Am J Pathol. 1986 Dec;125(3):578-84.
Two variants of coxsackievirus group B, Type 3 (CVB3o and CVB3M) infect Balb/c cardiac tissue equally, but only one variant (CVB3M) induces myocarditis. Various studies indicate that disease resistance in CVB3o-infected mice results from generation of suppressor cells. Low-dose cyclophosphamide (50 mg/kg body weight) treatment enhances inflammation in both CVB3M and CVB3o-infected animals, which clearly demonstrates that CVB3o has the capacity to induce disease, but inhibitory factors must exist preventing myocarditis. Spleen cells obtained from mice 10 days after CVB3o inoculation inhibited myocarditis induction in CVB3M-infected recipients, which confirms the presence of suppressor cells in these animals. The suppressor cell belongs to the Lyt 2+ subclass of T lymphocytes and specifically interferes with CVB3-induced myocarditis but fails to inhibit T-cell-mediated cardiac injury triggered by an unrelated virus, encephalomyocarditis virus.
B组柯萨奇病毒3型的两个变体（CVB3o和CVB3M）对Balb/c心脏组织的感染能力相同，但只有一个变体（CVB3M）会诱发心肌炎。多项研究表明，CVB3o感染的小鼠具有抗病能力是由于产生了抑制细胞。低剂量环磷酰胺（50毫克/千克体重）处理会增强CVB3M和CVB3o感染动物的炎症反应，这清楚地表明CVB3o具有诱发疾病的能力，但必定存在抑制因子来预防心肌炎。在接种CVB3o 10天后从小鼠获取的脾细胞抑制了CVB3M感染受体的心肌炎诱导，这证实了这些动物中存在抑制细胞。抑制细胞属于T淋巴细胞的Lyt 2+亚类，特异性干扰CVB3诱导的心肌炎，但不能抑制由无关病毒脑心肌炎病毒引发的T细胞介导的心脏损伤。
