Laurie A S, Gibson F M, Josten K M, Talbot P J, Rutherford T R, Lilleyman J S, Gordon-Smith E C
Department of Cellular and Molecular Sciences, St George's Hospital Medical School, London.
Br J Haematol. 1992 Apr;80(4):446-51. doi: 10.1111/j.1365-2141.1992.tb04556.x.
The pathogenesis of the neutropenia that occurs in some patients with chronic T cell lymphocytosis is not well understood. We have investigated a 15-year-old girl with this syndrome. Initial committed bone marrow progenitor numbers (CFUgm) were low but markedly increased in vitro following T cell depletion. Similarly a transient correction of neutropenia was observed following in vivo lymphocyte depletion with antilymphocyte globulin. A sustained neutrophil recovery was achieved with daily therapy using recombinant human granulocyte colony stimulating factor (rhG-CSF) despite persistence of the lymphocytosis; during successful therapy CFUgm numbers remained low, and were not increased by the in vitro addition of rhG-CSF. These observations suggest the possibility of an inhibitory regulatory mechanism specifically acting on neutrophil granulopoiesis.
部分慢性T细胞淋巴细胞增多症患者出现中性粒细胞减少的发病机制尚不清楚。我们研究了一名患有该综合征的15岁女孩。最初骨髓定向祖细胞数量（CFUgm）较低，但在T细胞去除后体外培养时显著增加。同样，在用抗淋巴细胞球蛋白进行体内淋巴细胞去除后，观察到中性粒细胞减少有短暂纠正。尽管淋巴细胞增多持续存在，但使用重组人粒细胞集落刺激因子（rhG-CSF）每日治疗仍实现了中性粒细胞的持续恢复；在成功治疗期间，CFUgm数量仍然较低，并且体外添加rhG-CSF后未增加。这些观察结果提示存在一种特异性作用于中性粒细胞生成的抑制性调节机制的可能性。
