Yang L C, Soprey P R, Wittner M K, Fox E N
J Exp Med. 1977 Aug 1;146(2):344-60. doi: 10.1084/jem.146.2.344.
We have demonstrated that T lymphocytes from the spleens of adult guinea pigs sensitized to group A streptococcal antigens are cytotoxic for cultured fetal guinea pig heart cells. Lymphocyte cytotoxicity, measured by 51Cr release from target cells, was stimulated by sensitization in vivo with group A whole cells, cell walls, and purified protoplast membranes emulsified with complete Freund's adjuvant (CFA). Sensitization with group C streptococcal antigens in CFA or CFA alone produced lymphocytes with little or no specific cytotoxic activity. Target cells of cultured fetal skeletal muscle, liver, or skin were relatively refractory to effector cell cytotoxicity. The presence of antigenic determinants on the membranes of cultured myofibers, cross-reacting with group A streptococcal cellular antigens, was confirmed by immunofluorescence. These data are discussed in terms of a model for poststreptococcal rheumatic myocarditis in which cell-mediated autoimmune mechanisms may participate.
我们已经证明,来自对A组链球菌抗原致敏的成年豚鼠脾脏的T淋巴细胞,对培养的豚鼠胎儿心脏细胞具有细胞毒性。通过靶细胞释放⁵¹Cr来测定淋巴细胞细胞毒性,用A组全细胞、细胞壁和用完全弗氏佐剂(CFA)乳化的纯化原生质体膜在体内致敏可刺激这种毒性。用C组链球菌抗原在CFA中致敏或仅用CFA致敏产生的淋巴细胞几乎没有或没有特异性细胞毒性活性。培养的胎儿骨骼肌、肝脏或皮肤的靶细胞对效应细胞的细胞毒性相对不敏感。通过免疫荧光证实,培养的肌纤维膜上存在与A组链球菌细胞抗原发生交叉反应的抗原决定簇。这些数据根据链球菌感染后风湿性心肌炎的模型进行了讨论,在该模型中细胞介导的自身免疫机制可能参与其中。