Hang L, Stephen-Larson P M, Henry J P, Dixon F J
Am J Pathol. 1984 Apr;115(1):42-6.
Among early life SLE mice, the male F1 hybrids of NZW X BXSB crosses are unique by their much earlier onset of glomerulonephritis (GN) (evident by 2 1/2 months of age), progressive hypertension, and high frequency of degenerative cardiovascular disease (CVD) with myocardial infarcts. In contrast, their female counterparts and the other kinds of SLE mice have later onset of GN, minimal hypertension, and lower incidence of CVD. The etiopathogenesis of these F1 males' disease was investigated by reciprocally transferring syngeneic lymphoid cells into lethally irradiated F1 male and female mice. As a result, female recipients of male lymphoid cells developed accelerated GN, hypertension, and severe CVD, but the male recipients of female lymphoid cells (at comparable ages) had delayed SLE, remained normotensive, and were spared coronary or myocardial damage. These findings strongly indicate that the hypertension and CVD of these F1 males originate from immunologic abnormalities rather than from other nonlymphoid factors.
在幼年SLE小鼠中，NZW与BXSB杂交的雄性F1代杂种具有独特性，它们的肾小球肾炎（GN）发病要早得多（2个半月龄时明显可见），伴有进行性高血压，且患有伴有心肌梗死的退行性心血管疾病（CVD）的频率很高。相比之下，它们的雌性对应物以及其他种类的SLE小鼠GN发病较晚，高血压程度较轻，CVD发病率较低。通过将同基因淋巴细胞相互转移到经致死性照射的F1代雄性和雌性小鼠中，对这些F1代雄性小鼠疾病的病因发病机制进行了研究。结果，接受雄性淋巴细胞的雌性受体出现了加速的GN、高血压和严重的CVD，但（在相当年龄）接受雌性淋巴细胞的雄性受体SLE发病延迟，血压保持正常，且未出现冠状动脉或心肌损伤。这些发现有力地表明，这些F1代雄性小鼠的高血压和CVD源自免疫异常，而非其他非淋巴因子。
