Abdou N I, NaPombejara C, Balentine L, Abdou N L
J Clin Invest. 1978 Mar;61(3):738-43. doi: 10.1172/JCI108987.
The mechanism of neutropenia in Felty's Syndrome (FS) was tested. The suppressor capacity of mononuclear cells from patients with FS on normal bone marrow granulopoiesis was tested by the in vitro colony forming unit in culture assay. Peripheral blood, bone marrow, and spleen cells from FS patients with marked neutropenia (less than 1,000 neutrophils/mm3) suppressed the colony forming unit in culture of normal bone marrow. Cells from rheumatoid arthritis patients without neutropenia, cells from patients with drug-induced neutropenia without rheumatoid arthritis, or plasma from FS patients failed to suppress the colony forming unit in culture. Though suppressor cells were predominantly thymus-derived (T) cells, monocytes were also effective in suppression. The suppressor efficiency of cells from the various compartments were spleen greater than bone marrow greater than peripheral blood. Splenectomy in FS transiently corrected the neutropenia and eliminated suppressor cell activity. Hyperactive suppressor cells may be responsible for the neutropenia in some patients with FS. Correction of neutropenia in these patients should be directed at modulating the suppressor cell subpopulation.
对费尔蒂综合征(FS)中性粒细胞减少的机制进行了检测。通过体外培养集落形成单位试验,检测了FS患者单核细胞对正常骨髓粒细胞生成的抑制能力。来自中性粒细胞显著减少(低于1000个中性粒细胞/mm³)的FS患者的外周血、骨髓和脾细胞抑制了正常骨髓的培养集落形成单位。无中性粒细胞减少的类风湿关节炎患者的细胞、无类风湿关节炎的药物性中性粒细胞减少患者的细胞或FS患者的血浆均未能抑制培养中的集落形成单位。虽然抑制细胞主要是胸腺来源的(T)细胞,但单核细胞也具有有效的抑制作用。来自不同部位的细胞的抑制效率为脾>骨髓>外周血。FS患者行脾切除术后可短暂纠正中性粒细胞减少并消除抑制细胞活性。某些FS患者的中性粒细胞减少可能与抑制细胞过度活跃有关。这些患者中性粒细胞减少的纠正应针对调节抑制细胞亚群。