论文部分内容阅读
目的:观察系统性红斑狼疮(SLE)患者血清IgG类抗体体外造血抑制活性及其与造血细胞过度凋亡的关系。方法:应用甲基纤维素集落培养法、原位末端标记及流式细胞术观察系统性红斑狼疮患者血清IgG在体外抑制正常骨髓造血干/祖细胞的增殖及促进正常CD34+细胞的凋亡。结果:活动期SLE患者血清IgG体外可明显抑制正常骨髓粒-巨噬系祖细胞(CFU-GM)和红系祖细胞(CFU-E)的增殖。这种IgG可特异吸附于正常CD34+细胞表面,加速CD34+细胞凋亡,上调CD34+细胞Fas抗原表达水平。结论:活动期SLE患者血清IgG在体外可抑制正常骨髓造血干/祖细胞的增殖。机制与其上调CD34+Fas抗原表达水平而促进CD34+细胞凋亡有关。
OBJECTIVE: To observe the in vitro hematopoietic inhibitory activity of serum IgG antibodies in patients with systemic lupus erythematosus (SLE) and its relationship with excessive apoptosis of hematopoietic cells. Methods: The serum IgG of patients with systemic lupus erythematosus (SLE) was detected by methylcellulose colony culture, end-site labeling and flow cytometry in vitro to inhibit the proliferation of normal bone marrow hematopoietic stem / progenitor cells and promote the apoptosis of normal CD34 + cells. Results: Serum IgG from patients with active SLE significantly inhibited the proliferation of normal myeloid granulocyte-macrophage-derived progenitor cells (CFU-GM) and erythroid progenitor cells (CFU-E) in vitro. The IgG could specifically adsorb on the surface of normal CD34 + cells, accelerate the apoptosis of CD34 + cells and upregulate the expression of Fas antigen in CD34 + cells. Conclusion: Serum IgG in active SLE patients can inhibit the proliferation of normal bone marrow hematopoietic stem / progenitor cells in vitro. Mechanism and its upregulation of CD34 + Fas antigen expression and promote CD34 + cell apoptosis.