Stollerman G H
Boston University, Boston, Massachusetts 02215.
Clin Immunol Immunopathol. 1991 Nov;61(2 Pt 1):131-42. doi: 10.1016/s0090-1229(05)80019-4.
The uniqueness of the group A streptococcus in initiating a cardiodestructive disease in a limited segment of the human species, regardless of race or ethnic group, makes the quest for a unique host response to a specific streptococcal antigen an intriguing and persisting challenge for clinical investigators, particularly for those investigators interested in autoimmunity. New methodology is making possible more incisive research approaches. The defined streptococcal antigens that turn out to be epitopes identical with host tissues, such as the M protein/cardiac myosin model or the hyaluronate in the capsule of mucoid rheumatogenic strains, offer the opportunity for more incisive clinical investigations. The isolation and cultivation of cardiotoxic T cell clones directed against such epitopes shared by host and parasite may eventually be possible. We may then learn more about whether autoimmunity is indeed a factor in the pathogenesis of rheumatic heart disease.
A 组链球菌能够在人类的一个特定亚群中引发心脏破坏性疾病，而不论其种族或族群如何，这一独特性使得探寻针对特定链球菌抗原的独特宿主反应成为临床研究人员，尤其是那些对自身免疫感兴趣的研究人员面临的一个引人入胜且持续存在的挑战。新方法使得更具洞察力的研究途径成为可能。已确定的链球菌抗原，如 M 蛋白/心肌肌球蛋白模型或黏液样致风湿菌株荚膜中的透明质酸，其表位与宿主组织相同，这为更具洞察力的临床研究提供了机会。针对宿主与病原体共有的此类表位的心脏毒性 T 细胞克隆的分离和培养最终或许可行。届时，我们可能会更多地了解自身免疫是否确实是风湿性心脏病发病机制中的一个因素。
