Fukuta S, Yoshinaga T, Yamakawa K, Kimura Y, Kusukawa R
Department of Internal Medicine, Yamaguchi University School of Medicine, Ube, Japan.
Jpn Circ J. 1992 Oct;56(10):1073-80. doi: 10.1253/jcj.56.1073.
The question of whether the etiology of DCM is immune or autoimmune has been increasingly discussed. Abnormal findings on humoral immunity in DCM were investigated, especially those regarding anti-heart antibodies (AHA), IgG subclasses and soluble interleukin-2 receptor (sIL-2R). The heterophile type AHA was detected in 64.7% of cases by the indirect immunofluorescence technique (IF) with rat heart, by indirect IF with human heart AHA in 57.8% of cases, and by thin-layer chromatogram with human glycolipids AHA in 44% of cases. Also, 57.1% of the specimens were found to bind IgG on perimyocytes by direct IF with biopsy specimens taken from patients with DCM. The epitope of an antigen which reacted with the heterophile type AHA is a Gal alpha 1-3Gal structure. 200 Kd, 70 Kd and 40 Kd antigens were reacted with AHA detected by indirect IF with human heart. The possible mechanisms of AHA in the pathogenesis could be either complement dependent cytotoxicity or interference to cardiac metabolism. The concentration of sIL-2R and IgG3 in sera from patients with DCM were elevated. These results suggest that immunological abnormalities occur continuously in DCM.
扩张型心肌病（DCM）的病因是免疫性还是自身免疫性的问题一直备受讨论。人们研究了DCM患者体液免疫的异常表现，尤其是抗心脏抗体（AHA）、IgG亚类和可溶性白细胞介素-2受体（sIL-2R）方面。通过大鼠心脏间接免疫荧光技术（IF）检测到64.7%的病例存在嗜异性AHA，通过人心脏AHA间接IF检测到57.8%的病例存在嗜异性AHA，通过人糖脂AHA薄层色谱法检测到44%的病例存在嗜异性AHA。此外，通过对DCM患者活检标本进行直接IF检测发现，57.1%的标本在心肌细胞周围结合IgG。与嗜异性AHA反应的抗原表位是Galα1-3Gal结构。通过人心脏间接IF检测到的AHA与200 Kd、70 Kd和40 Kd抗原发生反应。AHA在发病机制中的可能机制可能是补体依赖性细胞毒性或对心脏代谢的干扰。DCM患者血清中sIL-2R和IgG3的浓度升高。这些结果表明DCM中持续存在免疫异常。
