慢性粒细胞白血病骨髓巨噬细胞表达与细胞因子的相关性

发布时间：2018-03-23 09:47

本文选题：慢性粒细胞白血病　切入点：巨噬细胞　出处：《广东医学》2017年05期 　论文类型：期刊论文

【摘要】：目的探讨慢性粒细胞白血病(CML)患者骨髓中巨噬细胞及白细胞介素(IL)-1β、IL-2、IL-4、IL-10、γ干扰素(INF-γ)的表达及相关性以明确其临床意义。方法选择CML慢性期30例(CML-CP组)、加速期21例(CML-AP组)、急变期20例(CML-BP组)、经治疗后完全缓解的患者44例、未缓解7例以及30例缺铁性贫血患者(对照组),采用免疫组化染色法检测上述各组患者骨髓组织中CD68、CD163的表达变化;应用流式细胞仪分析相应患者骨髓IL-1β、IL-2、IL-4、IL-10、INF-γ表达;比较骨髓巨噬细胞在CML患者不同时期骨髓组织CD68、CD163的表达差异与IL-1β、IL-2、IL-4、IL-10、INF-γ表达变化的关系。结果 CML各组患者骨髓组织中CD68、CD163均有不同程度的表达,且随着病情的进展表达逐渐增高,即对照组CML-CP组CMLAP组CML-BP组,组间比较差异有统计学意义(P0.05);同时,CD163与CD68阳性细胞数密切相关(P0.05)。与对照组比较,CML-CP组骨髓IL-2、INF-γ明显降低(P0.05),IL-1β、IL-4、IL-10表达明显升高(P0.05);随着病情进展,IL-2、INF-γ表达逐渐降低,即对照组CML-CP组CML-AP组CML-BP组,其组间差异有统计学意义(P0.05),且与CD163表达呈负相关;IL-1β、IL-4、IL-10表达逐渐升高,对照组CML-CP组CML-AP组CML-BP组,组间差异有统计学意义(P0.05),并与CD163表达呈正相关。患者经治疗完全缓解后,CD68及CD163仍高于对照组(P0.05);IL-2、INF-γ有所回升,但仍低于对照组(P0.05),IL-1β、IL-4、IL-10有所降低,同样也高于对照组(P0.05)。未缓解组所测指标与CML-BP组相比,差异无统计学意义(P0.05)。结论巨噬细胞在CML患者骨髓中的异常浸润并逐渐从M1型向M2型巨噬细胞激化及IL-1β、IL-2、IL-4、IL-10、INF-γ的异常表达,改变了正常骨髓微环境,有利于白血病细胞的生存和增殖分化,可能与CML的发生、发展相关。
[Abstract]:Objective to investigate the expression and correlation of macrophage and IL-2IL-4IL-10, interferon 纬 (IFN- 纬) in bone marrow of patients with chronic myelogenous leukemia (CML). Methods 30 cases of chronic CML with CML-CP and 21 cases of accelerated stage with CML-AP were selected. There were 20 cases of CML-BP group and 44 cases of complete remission after treatment. The expression of CD68 ~ + CD163 in bone marrow of 7 patients without remission and 30 patients with iron deficiency anemia (control group) was detected by immunohistochemical staining, and the expression of IL-1 尾 -2IL-4IL-4IL-4IL-10 / INF- 纬 in bone marrow was analyzed by flow cytometry. To compare the relationship between the expression of CD68 / CD163 in bone marrow tissue of CML patients and the expression of IL-1 尾 -IL-2mIL-4 / IL-10 / INF- 纬 in bone marrow tissue of patients with CML. Results the expression of CD68 / CD163 in bone marrow tissue of CML patients was increased gradually with the progression of the disease. There was a significant difference between the CML-BP group and the control group (P 0.05), while CD163 was closely related to the number of CD68 positive cells. Compared with the control group, the expression of IL-2INF- 纬 in the bone marrow of the CML-CP group was significantly lower than that in the control group, and the expression of IL-4 IL-10 in the bone marrow of the CML-CP group was significantly higher than that in the control group, and the expression of IL-2INF- 纬 decreased gradually with the progression of the disease. The difference between CML-BP group and CML-CP group was statistically significant (P 0.05), and the expression of IL-10 was negatively correlated with the expression of IL-1 尾, IL-4 and IL-10 in CML-BP group, and the CML-BP group in CML-AP group in CML-CP group, and the expression of IL-10 in CML-BP group was significantly higher than that in control group (P < 0.05). The difference between the two groups was statistically significant and positively correlated with the expression of CD163. After complete remission, the levels of CD68 and CD163 in the patients were still higher than those in the control group (P 0.05), and the levels of IL-2INF- 纬 were higher than those in the control group, but they were still lower than those in the control group. It was also higher than the control group (P 0.05). There was no significant difference in the indexes measured between the non-remission group and the CML-BP group. Conclusion the abnormal infiltration of macrophages in the bone marrow of CML patients and the gradual aggravation from M1 type to M2 type macrophage and the abnormal expression of IL-1 尾 IL-2mIL-4 IL-4 IL-10 IL-10 INF- 纬 in the bone marrow of patients with CML. The change of normal bone marrow microenvironment is beneficial to the survival and proliferation and differentiation of leukemic cells, which may be related to the occurrence and development of CML.
【作者单位】：云南省第一人民医院血液学诊断室;云南省第一人民医院血液科;云南省第一人民医院临床基础研究所;
【基金】：国家自然科学基金资助项目(编号:31460298) 云南省科技厅-昆明医科大学联合专项应用基础研究项目资助(编号:2014FZ070)
【分类号】：R733.72

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