Denman A M, Denman E J
Clin Exp Immunol. 1970 Apr;6(4):457-72.
Labelling studies with tritiated thymidine in NZB mice revealed that old mice of this strain with established Coombs positive haemolytic anaemia were depleted predominantly of long-lived small lymphocytes. Lymphopoiesis in the bonemarrow was relatively less affected suggesting that the peripheral destruction or deviation of re-circulating lymphocytes and not a precursor cell deficiency may account for the depletion of these cells. Old NZB mice in which the development of Coombs positive haemolytic anaemia, but not other disease features, has been prevented by thymectomy and treatment with anti-lymphocyte globulin several months earlier were equally deficient in this population of lymphocytes. C57BL mice, subjected to the same regime largely regenerated this population during the subsequent 12 months and rejected skin homografts in the same time as young controls of the same strain. Loss of lymphocytes responsible for antigen recognition would account for the impaired cellular immunity of old NZB mice observed in this study and described earlier by other authors. This process appears to accompany the progression of the spontaneous disease in this strain.
用氚标记的胸腺嘧啶核苷对新西兰黑鼠进行的标记研究表明,患有已确诊的库姆斯阳性溶血性贫血的该品系老年鼠,主要是长寿命小淋巴细胞数量减少。骨髓中的淋巴细胞生成相对受影响较小,这表明循环淋巴细胞的外周破坏或偏离,而非前体细胞缺乏,可能是这些细胞数量减少的原因。几个月前通过胸腺切除和抗淋巴细胞球蛋白治疗预防了库姆斯阳性溶血性贫血(但未预防其他疾病特征)发展的老年新西兰黑鼠,在这一淋巴细胞群体中同样存在缺陷。接受相同处理的C57BL小鼠在随后的12个月里该群体大量再生,并在与同品系年轻对照相同的时间内排斥皮肤同种异体移植。负责抗原识别的淋巴细胞缺失可解释本研究中观察到的老年新西兰黑鼠细胞免疫受损现象,其他作者此前也对此进行过描述。这一过程似乎伴随着该品系自发性疾病的进展。