Morra L, Ponassi A G, Gurreri G, Moccia F, Mela G S, Bogliolo F, Beltrami P, Sacchetti C
Istituto Scientifico di Medicina Interna, Università di Genova, Italia.
Acta Haematol. 1988;79(4):187-91. doi: 10.1159/000205805.
The growth of normal burst-forming units (BFU-E) is known to depend on a burst-promoting activity (BPA) produced by T-lymphocytes. Few BFU-E colonies have been observed in cultures of blood mononuclear cells (MNC) of uremic patients. The aim of the present study was to examine the concentration of BFU-E in the blood of uremic patients and to evaluate the ability of uremic T-lymphocytes to produce BPA. We have studied 6 chronic uremic patients treated with maintenance hemodialysis. When 5 X 10(5) blood MNC depleted of T-lymphocytes of uremic subjects were stimulated by 1 X 10(6) normal T-lymphocytes in a methylcellulose culture system we observed the growth of a number of BFU-E colonies that did not differ significantly from normal (29 +/- 11.8 colonies). On the contrary, when 5 X 10(5) blood MNC depleted of T-lymphocytes of normal subjects were stimulated by 1 X 10(6) T-lymphocytes of uremic patients, the number of BFU-E colonies obtained was significantly lower than normal (1.9 +/- 3.1 colonies). These data show that the decreased number of BFU-E colonies obtained from blood MNC of uremic patients is due to a defect of uremic T-lymphocytes. The impairment of T-lymphocytes can be due to inhibitors of T-lymphocyte function or to variations in T cell subsets, leading to a decrease in the OKT4/OKT8 cell ratio. In any case it is a significant pathogenetic mechanism contributing to anemia in chronic uremia.
已知正常爆式红系集落形成单位（BFU-E）的生长依赖于T淋巴细胞产生的爆式促进活性（BPA）。在尿毒症患者的血液单核细胞（MNC）培养物中观察到的BFU-E集落很少。本研究的目的是检测尿毒症患者血液中BFU-E的浓度，并评估尿毒症T淋巴细胞产生BPA的能力。我们研究了6例接受维持性血液透析治疗的慢性尿毒症患者。在甲基纤维素培养系统中，当用1×10⁶个正常T淋巴细胞刺激5×10⁵个去除尿毒症患者T淋巴细胞的血液MNC时，我们观察到一些BFU-E集落的生长，其与正常情况无显著差异（29±11.8个集落）。相反，当用1×10⁶个尿毒症患者的T淋巴细胞刺激5×10⁵个去除正常受试者T淋巴细胞的血液MNC时，获得的BFU-E集落数量显著低于正常水平（1.9±3.1个集落）。这些数据表明，从尿毒症患者血液MNC中获得的BFU-E集落数量减少是由于尿毒症T淋巴细胞的缺陷所致。T淋巴细胞的损伤可能是由于T淋巴细胞功能抑制剂或T细胞亚群的变化，导致OKT4/OKT8细胞比值降低。无论如何，这是导致慢性尿毒症贫血的一个重要发病机制。
