摘要
目的通过检测慢性再生障碍性贫血(CAA)患者骨髓单个核细胞(MNC)雄激素受体(AR)以及骨髓中活化T抑制细胞水平,探讨雄激素受体在CAA免疫病理机制中的作用。方法①免疫细胞化学SP法检测CAA骨髓MNC胞浆和胞核内AR的阳性表达水平;②流式细胞术检测CAA骨髓中T细胞亚群(CD3+CD4+细胞、CD3+CD8+细胞)和活化T抑制细胞(CD8+CD25+细胞、CD8+HLA-DR+细胞)的含量。结果①CAA患者骨髓MNC胞浆和胞核内AR阳性水平(38.18±4.47)显著低于对照组(52.44±6.71)(个/200个MNC);不同性别间AR的含量未见显著差异。②CAA患者骨髓中的CD3+CD8+细胞、CD8+HLA-DR+细胞含量分别为(28.66±3.75)%和(24.43±4.16)%,均显著高于对照组;而二组中骨髓内的CD3+CD4+细胞、CD8+CD25+细胞均未见显著差异。③CAA患者骨髓中的AR阳性水平与骨髓中的CD3+CD8+细胞呈负相关,r=-0.553,P<0.01;而与CD8+HLA-DR+、CD3+CD4+、CD8+CD25+细胞含量未见明显的直线相关关系。结论CAA患者AR的表达减少,从而使雄激素刺激骨髓造血的作用减弱。患者AR的表达与CD3+CD8+细胞含量呈明显负相关,表明雄激素受体的异常可能在一定程度上参与了慢性再生障碍性贫血发病机制中的细胞免疫异常。
Objective To study the role of androgen receptor in immuno-pathogenesis of chronic aplastic anemia. Methods ① Immunocytochemical technique was used to evaluate the expression of androgen receptor in nuclear and plasma of bone marrow mononuclear cells in 26 chronic aplastic anemia patients and 25 healthy controls. ②Flow cytometry was used to evaluate the contents of T- lymphocyte subsets（CD3^＋ CD4^＋ cells, CD3^＋ CD8^＋ cells） and activated Ts lymphocytes（CD8^＋ CD25^＋ cells, CD8^＋ HLA-DR^＋ cells） in bone marrow mononuclear cells. Results The expression of androgen receptor in bone marrow in newly diagnosed group was significantly lower than that in control group. The contents of CD3^＋ CD8^＋ and CD8^＋ HLA-DR^＋ lymphocytes in newly diagnosed group were significantly higher than those in control group, while there was no significant difference in CD3^＋ CD4^＋ cells and CD8^＋ CD25^＋ cells between two groups. In addition, the expression of androgen receptor in bone marrow had a negative relationship with CD3^＋CD8^＋ lymphocytes in bone marrow. Conclusion The lower expression of androgen receptor in CAA patients induces the weaker stimulation of androgen to hematopoiesis in bone marrow. The AR expression in patients has a negative relationship with the contents of CD3^＋CD8^＋ lymphocytes, suggesting the abnormality of androgen receptor might have a role in the abnormality of cellular immunity in pathogenesis of chronic aplastic anemia.
出处
《山西医科大学学报》
CAS
2006年第5期474-476,共3页
Journal of Shanxi Medical University
基金
山西省高校科技开发研究基金资助项目(2003117)
