Lunardi-Iskandar Y, Georgoulias V, Vittecoq D, Ammar A, Rozenbaum W, Meyer P, Jasmin C
Unité d'Oncogénèse Appliquée (INSERM U 268), Villejuif, France.
Biomed Pharmacother. 1988;42(1):21-9.
The in vitro proliferation capacity of peripheral blood committed T-cell precursors (T-CFC) from LAS patients was studied in order to define whether this parameter could be associated with transition to AIDS. In all patients a significantly (P less than 0.0001) decreased plating efficiency was detected. However, the lowest T-cell colony growth (less than 50 colonies/5 x 10(4) cells) was observed in the 23 patients who subsequently developed the full-blown disease within 150-570 days. Conversely, only one patient (n = 107) whose T-CFC generated greater than 50 colonies/5 x 10(4) cells developed AIDS after a mean follow-up of 867 days (range 120-1260 days). T-CFC from these patients displayed an impaired in vitro differentiation and self-renewal capacity which was independent of the clinical evolution of the disease. In 5 out of 12 AIDS patients, adherent cell-depletion of peripheral blood mononuclear cells (PBMC) enhanced the plating efficiency. Moreover, patients' but not normal adherent cells could inhibit normal T-cell colony growth in a dose-dependent manner. Media conditioned by patients' unstimulated adherent cells (LCM-A+p) also inhibited normal T-cell colony formation. In addition, LCM-A+p were capable of inhibiting interleukin 2-receptor (IL 2-R) expression and interleukin 2 (IL 2) production by normal mitogen-stimulated T-cells. These findings suggest that adherent cell-derived inhibitory activity(ies) could be responsible for the low T-cell colony formation observed in some AIDS patients.
为了确定外周血定向T细胞前体(T-CFC)的体外增殖能力是否与向艾滋病的转变有关,对LAS患者的该指标进行了研究。在所有患者中均检测到接种效率显著降低(P小于0.0001)。然而,在随后150-570天内发展为典型疾病的23例患者中,观察到最低的T细胞集落生长(小于50个集落/5×10⁴个细胞)。相反,在平均随访867天(范围120-1260天)后,T-CFC产生大于50个集落/5×10⁴个细胞的患者中,只有1例(n = 107)发展为艾滋病。这些患者的T-CFC显示出体外分化和自我更新能力受损,这与疾病的临床进展无关。在12例艾滋病患者中的5例中,外周血单个核细胞(PBMC)的贴壁细胞去除增强了接种效率。此外,患者的贴壁细胞而非正常贴壁细胞能够以剂量依赖的方式抑制正常T细胞集落生长。患者未刺激的贴壁细胞条件培养基(LCM-A+p)也抑制正常T细胞集落形成。此外,LCM-A+p能够抑制正常有丝分裂原刺激的T细胞的白细胞介素2受体(IL-2-R)表达和白细胞介素2(IL-2)产生。这些发现表明,贴壁细胞衍生的抑制活性可能是某些艾滋病患者中观察到的低T细胞集落形成的原因。