Maisch B
Heart Vessels. 1986;2(1):55-9. doi: 10.1007/BF02060247.
Sera and lymphocytes from a 37-year-old male patient with acute perimyocarditis during a Q-fever endemic were analyzed for antibody and cell-mediated immune reactions and followed up 28 months later. Circulating autoantibodies against myocardial tissue were assessed by indirect immunofluorescence. Cytolysis of vital contracting rat cardiocytes, by antimyolemmal antibodies and complement, and lymphocytotoxicity, with and without the patient's serum, were evaluated and compared with the results obtained in ten patients suffering from Q-fever without perimyocardial involvement and with 40 healthy subjects. Antimyolemmal antibodies (AMLA), a muscle-specific subtype of antisarcolemmal antibodies, were demonstrated by immunofluorescence in the one patient with Q-fever perimyocarditis in titers of up to 1:320 but not in the controls. AMLA induced cytolysis of myocytes in the presence of complement. Both AMLA and cytolytic serum activity could be absorbed in all sera of this patient by using Coxiella burnetii. Only marginal lymphocytotoxicity against heterologous cardiocytes was detected in the early phase and again during the follow-up 2 years later in the Q-fever myocarditis patient but not in any of the noncarditic Q-fever cases nor in controls. It is postulated that cross-reacting, complement-fixing, cytolytic autoantibodies against the cardiac myolemma are operative either as a cause of cardiac damage or a consequence, pointing to a secondary immunopathogenesis of chronic Q-fever perimyocarditis.
对一名37岁男性急性心包心肌炎患者在Q热流行期间的血清和淋巴细胞进行了抗体和细胞介导免疫反应分析，并在28个月后进行了随访。通过间接免疫荧光评估针对心肌组织的循环自身抗体。评估了抗肌膜抗体和补体对活的收缩大鼠心肌细胞的细胞溶解作用，以及有无患者血清时的淋巴细胞毒性，并与10名无心肌受累的Q热患者和40名健康受试者的结果进行了比较。通过免疫荧光在1例Q热心包心肌炎患者中检测到抗肌膜抗体（AMLA），这是抗肌膜抗体的一种肌肉特异性亚型，滴度高达1:320，而在对照组中未检测到。AMLA在补体存在下可诱导心肌细胞溶解。使用伯氏考克斯体可吸收该患者所有血清中的AMLA和细胞溶解血清活性。在Q热心肌炎患者的早期以及2年后的随访中仅检测到对异源性心肌细胞的轻微淋巴细胞毒性，而在任何非心脏Q热病例或对照组中均未检测到。据推测，针对心肌肌膜的交叉反应性、补体固定性、细胞溶解性自身抗体可能是心脏损伤的原因或结果，提示慢性Q热心包心肌炎的继发性免疫发病机制。
