Maisch B
Department of Internal Medicine, Cardiology, Philipps-University Marburg, FRG.
Thorac Cardiovasc Surg. 1990 Aug;38 Suppl 2:157-63. doi: 10.1055/s-2007-1014059.
Whereas abundant literature is available on mechanisms imposed by neoplastic diseases on the immune system, only few details are known about immunological parameters of autoreactive mechanisms directed against the heart. This report will focus on cardiac autoreactivity in patients with endomyocardial types of cardiac tumors (e.g. atrial myxomas), Hodgkin's disease, and with neoplastic pericardial effusion. In patients with atrial myxomas antimyolemmal antibodies were significantly increased when compared to non-cardiac controls. Antisarcolemmal antibodies were positive in 100% of trivalent immunoglobulin binding. Antiendothelial antibodies of the IgG type could be found in 86% of patients with atrial myxoma. Circulating immune complexes were present in 6 out of 7 patients. In 107 patients with Hodgkin's disease without pericarditis the presence of antimyolemmal antibodies was lower than in healthy controls. The incidence of antimyolemmal antibodies in 10 patients with pericarditis lymphogranulomatosa was 10%, whereas in postradiation pericarditis 8 of 15 patients demonstrated antimyolemmal antibodies. Antiendothelial antibodies were positive in 7 out of 15 patients. The number of patient lymphocytes available for functional assays is yet too small to permit further conclusions on cellular autoreactive mechanisms in Hodgkin's disease. Antimyocardial antibodies were found both in the serum and in the effusions at least in lower titers in all patients. With regard to in-vitro analysis it can not be excluded that a balance between protective and cytolytic antibodies keeps a normal mean of antibody-mediated cytolysis. Analysing the first line of defense, the natural killer cell activity was found significantly increased in neoplastic pericardial effusions, whereas peripheral blood and pericardial effusion showed no lymphocytotoxicity with isolated myocardial cells.
尽管有大量关于肿瘤疾病对免疫系统影响机制的文献,但针对心脏的自身反应性机制的免疫学参数却知之甚少。本报告将聚焦于心内膜型心脏肿瘤(如心房黏液瘤)、霍奇金病以及伴有肿瘤性心包积液患者的心脏自身反应性。与非心脏对照相比,心房黏液瘤患者的抗肌膜抗体显著增加。在三价免疫球蛋白结合检测中,抗肌膜抗体的阳性率为100%。86%的心房黏液瘤患者可检测到IgG型抗内皮细胞抗体。7例患者中有6例存在循环免疫复合物。107例无心包炎的霍奇金病患者中,抗肌膜抗体的阳性率低于健康对照。10例淋巴肉芽肿性心包炎患者中抗肌膜抗体的发生率为10%,而在放射性心包炎患者中,15例中有8例检测到抗肌膜抗体。15例患者中有7例抗内皮细胞抗体呈阳性。可用于功能检测的患者淋巴细胞数量过少,无法就霍奇金病中的细胞自身反应性机制得出进一步结论。至少在所有患者的血清和积液中均检测到低滴度的抗心肌抗体。关于体外分析,不能排除保护性抗体和细胞溶解抗体之间的平衡维持了抗体介导的细胞溶解的正常平均值。分析第一道防线,发现肿瘤性心包积液中的自然杀伤细胞活性显著增加,而外周血和心包积液对分离的心肌细胞均无淋巴细胞毒性。