Mezzano S, Pesce A J, Pollak V E, Michael J G
Nephron. 1984;36(1):15-9. doi: 10.1159/000183109.
An experimental model in rats was developed to define the nature of humoral and cellular factors that contribute to impaired immune responsiveness in chronic renal failure. Addition of uremic rat serum to both normal and uremic lymphocytes significantly suppressed cellular responses, the suppression being more pronounced with uremic lymphocytes. Lymphocytes from uremic rats were only marginally less responsive than normal lymphocytes to concanavalin A stimulation when normal rat serum was added to the cultures, indicating that the cellular factors in impairment were less important than humoral ones. Antibody formation in rat splenocyte cultures to bovine serum albumin was suppressed by addition of uremic serum, but the response to sheep erythrocytes was unaffected. Thus the effect on antibody response in uremic animals is dependent upon the antigen tested.
建立了一种大鼠实验模型，以确定导致慢性肾功能衰竭免疫反应受损的体液和细胞因子的性质。向正常和尿毒症淋巴细胞中添加尿毒症大鼠血清均显著抑制细胞反应，尿毒症淋巴细胞的抑制作用更为明显。当向培养物中添加正常大鼠血清时，尿毒症大鼠的淋巴细胞对刀豆蛋白A刺激的反应仅略低于正常淋巴细胞，这表明损伤中的细胞因子不如体液因子重要。向大鼠脾细胞培养物中添加尿毒症血清可抑制对牛血清白蛋白的抗体形成，但对绵羊红细胞的反应未受影响。因此，尿毒症动物对抗体反应的影响取决于所测试的抗原。
