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为探讨ＡＡ的免疫发病机制，阐明细胞因子在ＡＡ患者中变化的基础与临床意义，应用ＥＬＩＳＡ法及ＡＰＡＡＰ法对３８例初治ＡＡ患者及２０名正常人外周血单个核细胞（ＰＢＭＮＣ）培养上清诱生的Ｇ－ＣＳＦ、ＩＬ－６、ＴＮＦα、ＩＦＮα及ＩＬ－８进行检测，同时观察外周血象、Ｔ细胞亚群及ＨＬＡ－ＤＲ表达。结果：ＡＡ患者外周血ＣＤ４减低，ＣＤ８增高，ＣＤ４／ＣＤ８减低或倒置，ＨＬＡ－ＤＲ抗原表达率增高。ＡＡ患者ＰＢＭＮＣ培养上清中Ｇ－ＣＳＦ阳性率减低，ＩＬ－６、ＴＮＦα、ＩＦＮα及ＩＬ－８水平增高。Ｇ－ＣＳＦ与ＣＤ４及ＣＤ４／ＣＤ８呈正相关而与ＩＦＮα呈负相关，ＩＬ－６与白细胞数及ＣＤ４呈负相关，ＴＮＦα与ＣＤ８呈正相关而与ＣＤ４／ＣＤ８呈负相关，ＩＬ－８与ＣＤ８及ＨＬＡ－ＤＲ呈负相关，证明细胞免疫功能异常及细胞因子网络失调在ＡＡ发病中起重要作用，激活的ＣＤ８细胞可以抑制造血，多种因素引起的细胞因子紊乱最终引发ＡＡ。
To explore the pathogenesis of AA and elucidate the basic and clinical significance of the changes of cytokines in patients with AA, 38 cases of newly diagnosed AA patients and 20 normal PBMNCs were cultured by ELISA and APAAP The levels of G-CSF, IL-6, TNFα, IFNα and IL-8 were detected by ELISA. Peripheral blood samples, T cell subsets and HLA-DR expression were also observed. Results: In patients with AA, the CD4, CD8, CD4 / CD8 decreased or reversed, the expression of HLA-DR antigen increased. The positive rate of G-CSF in PBMNC culture supernatant of AA patients was decreased and the levels of IL-6, TNFα, IFNα and IL-8 were increased. G-CSF was positively correlated with CD4 and CD4 / CD8 but negatively correlated with IFNa. IL-6 was negatively correlated with leukocyte count and CD4. TNF-a positively correlated with CD8 but negatively correlated with CD4 / CD8. HLA-DR was negatively correlated to prove that abnormal cellular immune function and cytokine network disorders play an important role in the pathogenesis of AA, activated CD8 cells can inhibit hematopoiesis, a variety of factors caused by cytokines eventually lead to AA.