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目的探讨CD34+干／祖细胞与纤维连接蛋白（FN）的粘附在慢性粒细胞白血病（CML）发病中的作用。方法①采用流式细胞术双标记法检测初治CML慢性期30例和正常骨髓10份CD34+细胞上整合素β1链（CD29）和α4链（CD49d）的表达；②结晶紫染色法观察免疫磁珠分选的CML慢性期5例和5名正常人骨髓CD34+细胞与FN的粘附功能；③极限稀释液体微培养观察FN对正常和CML慢性期骨髓粒细胞-巨噬细胞祖细胞集落（CFU－GM）形成能力的影响。结果①CML慢性期骨髓CD34+细胞CD29和CD49d的表达与正常骨髓比较，差异无显著性；②CML骨髓CD34+细胞与FN的粘附明显低于正常（P＜0．01）；③FN显著抑制正常骨髓CFU-GM的形成（P＜0．01），而对CML骨髓CFU-GM的形成无显著影响。结论CML骨髓CD34+干／祖细胞与FN的粘附功能减弱，因而缺乏FN对祖细胞增殖的调节作用是CML髓系扩增的原因之一。
Objective To investigate the role of adhesion of CD34 + stem / progenitor cells to fibronectin (FN) in the pathogenesis of chronic myelogenous leukemia (CML). Methods ① The expression of integrin β1 chain (CD29) and α4 chain (CD49d) on 30 CD34 + cells in 30 newly diagnosed CML patients and 10 normal CD8 + CD8 + T cells were detected by flow cytometry. ② The immunofluorescence was observed by crystal violet staining Beads in the chronic phase of CML five cases and five normal human bone marrow CD34 + cells and FN adhesion function; ③ limit dilution liquid micro culture observed FN normal and CML chronic myeloid granulocyte-macrophage progenitor cells (CFU -GM) formation ability. Results ① The expression of CD29 and CD49d in chronic myelogenous leukemia CD34 + cells was not significantly different from that in normal bone marrow. ② The adhesion of CD34 + cells to FN in CML bone marrow was significantly lower than normal (P <0.01); ③FN significantly inhibited the expression of CFU- GM formation (P <0.01), but had no significant effect on the formation of CML bone marrow CFU-GM. Conclusion The adhesion function of CML bone marrow CD34 + stem / progenitor cells to FN is weakened. Therefore, the regulatory effect of FN on progenitor cell proliferation is one of the reasons of CML myeloid expansion.