rhG-CSF动员正常人外周血干细胞过程中对T淋巴细胞增殖的影响

目的　探讨rhG CSF体内对T淋巴细胞增殖影响的作用机制。方法　取行异基因造血干细胞移植的HLA相合的同胞供者应用rhG CSF前后的静脉血和单采物 ,用MTT法测定去除单核细胞前、后的外周血单个核细胞 (MNC)对PHA增殖反应的改变。用流式细胞术检测单核细胞绝对数的改变、抗原呈递细胞 (包括单核细胞和B淋巴细胞 )协同刺激因子CD80 (B7 1 )、CD86(B7 2 )的表达以及贴壁前、后CD1 4+细胞比例。结果　rhG CSF体内作用后 ,外周血中单核细胞绝对数升高了 (4.2 0± 1 .74)倍 ,T细胞在去除单核细胞后增殖能力部分恢复 ,但仍较G CSF作用前平均降低 2 0 .58%。单核细胞表达共刺激信号CD86下降了 (66 .96± 1 3 .87) % ,相对平均荧光强度降低了 (31 .31± 1 2 .91 ) % ,B淋巴细胞中表达CD80 降低了 (45 .77± 2 6 .58) %。结论　G CSF体内作用后 ,单核细胞数量的改变抑制T淋巴细胞增殖 ,但它并不能完全解释T淋巴细胞的反应低下 ,而单核细胞和B淋巴细胞表达低水平的B7分子 ,提示这些抗原提呈细胞功能的改变可能参与T淋巴细胞增殖改变

Study on the in vivo effect of rhG-CSF on peripheral T lymphocyte

OBJECTIVE: To investigate the mechanisms of in vivo rhG-CSF affecting T lymphocyte. METHODS: Peripheral blood and apheresis graft were obtained from sibling donors before and after G-CSF administration. Proliferation of peripheral blood mononuclear cells (MNC) stimulated by PHA before and after removing monocyte by plastic-adherence was detected by MTT test. Absolute number of MNC, costimulating molecules expression on antigen presenting cells (monocyte and B lymphocyte) and the number of CD(14)(+) cells before and after plastic-adherence treatment were analyzed by flow cytometry. RESULTS: After rhG-CSF administration, absolute peripheral blood monocyte counts increased by 4.2 +/- 1.74 times. By removing monocytes, proliferation of T cells after rhG-CSF administration partly restored, but remained 20.58% lower than that before G-CSF treatment. CD(86) co-stimulating factor expression on monocyte declined (66.96 +/- 13.87)% and mean fluorescence intensity (MIF) decreased (31.31 +/- 12.91)% after rhG-CSF administration. Expression of CD(80) on B lymphocyte decreased (45.77 +/- 26.58)%. CONCLUSIONS: The increased number of monocytes after rhG-CSF administration suppressed T-cell proliferation, which was partly the mechanism of the T-cell hyporesponsiveness. The fact that monocyte and B lymphocyte expressed low level of B(7) co-stimulating factor suggested that antigen present cells might also mediate the alteration of T-cell proliferation.