Inadequate Ability of T-Lymphocytes from Chronic Uremic Subjects to Stimulate the in vitro Growth of Committed Erythroid Progenitors (BFU-E)

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Abstract
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 mono-nuclear 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 × 105 blood MNC depleted of T-lymphocytes of uremic subjects were stimulated by 1 × 106 normal T-lymphocytes in a methylcel-lulose 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 × 105 blood MNC depleted of T-lymphocytes of normal subjects were stimulated by 1 × 106 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.