Maisch B, Bülowius U, Schmier K, Klopf D, Koper D, Sibelis T, Kochsiek K
Herz. 1985 Feb;10(1):8-14.
The diagnosis, pathogenesis and etiology of myocarditis are often difficult to establish with certainty. Consequently, we investigated cellular regulator and effector mechanisms in patients with viral heart disease (Coxsackie B3, influenza, EBV, mumps) as well as other inflammatory heart diseases which could not be classified etiologically. In acute myocarditis there was an elevation of B- and activated T-lymphocytes (OKIa 1-positive) but, in contrast, no significant changes in the activity of peripheral suppressor T-cells (OKT 8-positive). The activity of cell-specific lymphocytic effector mechanisms against vital cardiocytes was unchanged or slightly elevated in myocarditis, while the activity of the less target cell specific natural killer cells, which were measured in vitro against K562 tumor cells, was diminished. These findings are indicative of increased activity of target specific cytotoxic effector mechanisms and a reduction in the activity of nonspecific cellular effector mechanisms in peripheral blood.
心肌炎的诊断、发病机制和病因往往难以确切确定。因此，我们研究了病毒性心脏病（柯萨奇B3病毒、流感病毒、EB病毒、腮腺炎病毒）患者以及其他病因无法分类的炎症性心脏病患者的细胞调节和效应机制。在急性心肌炎中，B淋巴细胞和活化的T淋巴细胞（OKIa 1阳性）有所升高，但相比之下，外周抑制性T细胞（OKT 8阳性）的活性没有显著变化。在心肌炎中，针对重要心肌细胞的细胞特异性淋巴细胞效应机制的活性未改变或略有升高，而在体外针对K562肿瘤细胞测定的对靶细胞特异性较低的自然杀伤细胞的活性则降低。这些发现表明外周血中靶标特异性细胞毒性效应机制的活性增加，而非特异性细胞效应机制的活性降低。
