Blakley B R
Can J Comp Med. 1985 Jan;49(1):104-8.
Six week old BDF1 female mice were exposed to cadmium chloride in the drinking water at concentrations ranging from 0 to 50 micrograms/mL cadmium for three weeks. The humoral immune response against sheep red blood cells which is T-lymphocyte and macrophage dependent, was suppressed in a dose dependent fashion with the maximum suppression of 28.2% observed in the highest exposure group (P less than 0.0001). Mitogen studies demonstrated that cadmium was a weak mitogen, producing a dose-dependent enhancement of blastogenesis (P = 0.026). T-lymphocyte responses which were induced by concanavalin A were not affected by cadmium exposure (P = 0.284). A dose-dependent enhancement of the B-lymphocyte activity was produced in the presence of cadmium when the lymphocytes were induced with Escherichia coli, lipopolysaccharide, a B-lymphocyte mitogen (P = 0.007). These results suggest that the immunosuppressive effects of cadmium associated with the humoral immune response are not due to an impairment of lymphocyte proliferation, an intermediate step involved in the generation of an immune response. The immunosuppressive effects were produced at relatively low cadmium exposures as indicated by the renal cadmium concentrations suggesting that the immune systems is very vulnerable to the toxic effects of cadmium.
六周龄的BDF1雌性小鼠在饮用水中接触浓度范围为0至50微克/毫升镉的氯化镉，持续三周。针对绵羊红细胞的体液免疫反应依赖于T淋巴细胞和巨噬细胞，呈剂量依赖性抑制，在最高暴露组中观察到最大抑制率为28.2%（P小于0.0001）。丝裂原研究表明，镉是一种弱丝裂原，可产生剂量依赖性的母细胞生成增强（P = 0.026）。伴刀豆球蛋白A诱导的T淋巴细胞反应不受镉暴露影响（P = 0.284）。当用大肠杆菌、脂多糖（一种B淋巴细胞丝裂原）诱导淋巴细胞时，镉存在下会产生剂量依赖性的B淋巴细胞活性增强（P = 0.007）。这些结果表明，与体液免疫反应相关的镉的免疫抑制作用并非由于淋巴细胞增殖受损，而淋巴细胞增殖是免疫反应产生过程中的一个中间步骤。如肾脏镉浓度所示，在相对较低的镉暴露水平下就产生了免疫抑制作用，这表明免疫系统对镉的毒性作用非常敏感。
