Haubitz M, Klöppel B, Lonnemann G, Nonnast-Daniel B
Department of Nephrology, University Hospital Hannover, Germany.
Clin Nephrol. 1992 Jul;38(1):30-5.
A monocyte defect is thought to be involved in the impaired immune response in patients on regular hemodialysis therapy. As an indicator of cell function, we studied in vitro IL-1 beta production of mononuclear cells from hemodialysis patients in comparison to normal controls. Mononuclear cells were stimulated with endotoxin or Staphylococcus epidermidis in parallel with control incubations in tissue culture medium alone. Spontaneous as well as stimulated total IL-1 beta production (cell-associated plus extracellular) did not differ significantly in cells obtained from patients compared to those from normal controls. However, the relative amounts of IL-1 beta released into the cell supernatants were significantly reduced in mononuclear cells from hemodialysis patients when stimulated with endotoxin but not with Staphylococcus epidermidis. These data indicate a stimulus-dependent defect in the mechanism of IL-1 beta release. As IL-1 is necessary for T-cell activation this alteration in mononuclear cell function may play a role in the impaired cellular immunity observed in patients on chronic hemodialysis therapy.
单核细胞缺陷被认为与接受常规血液透析治疗的患者免疫反应受损有关。作为细胞功能的一个指标，我们研究了血液透析患者单核细胞的体外白细胞介素-1β（IL-1β）产生情况，并与正常对照进行比较。单核细胞用内毒素或表皮葡萄球菌刺激，同时设置仅在组织培养基中孵育的对照。与正常对照相比，患者来源的细胞自发以及受刺激后的总IL-1β产生量（细胞相关和细胞外）无显著差异。然而，当用内毒素而非表皮葡萄球菌刺激时，血液透析患者单核细胞释放到细胞上清液中的IL-1β相对量显著降低。这些数据表明IL-1β释放机制存在刺激依赖性缺陷。由于IL-1是T细胞活化所必需的，单核细胞功能的这种改变可能在慢性血液透析治疗患者中观察到的细胞免疫受损中起作用。
