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变应性鼻炎患者外周血单个核细胞Th_1/Th_2细胞因子的检测及其意义 被引量:3

Study on Th_1/Th_2 cytokines in peripheral blood mononuclear cells (PBMC) in patients with allergic rhinitis
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摘要 目的 :探讨T淋巴细胞活化及释放的Th1/Th2 细胞因子失平衡与变态反应性鼻炎发病的关系。方法 :用双抗体夹心酶联免疫吸附试验 (ELISA)测定 40例变态反应性鼻炎患者 ,2 0例慢性鼻炎患者和 2 0例健康人的外周血单个核细胞 (PBMC) ,经PHA诱导培养后上清液中Th1细胞因子γ干扰素 (IFN -γ)和Th2 细胞因子白介素 4(IL -4)、白介素 5 (IL -5 )的水平及血清中可溶性白介素 2受体 (sIL -2R)的水平 ,并分别对变应性鼻炎患者的sIL -2R与IFN -γ、IL-4、IL -5的相关性进行研究。结果 :PBMC培养的上清液中变应性鼻炎组的IL -4和IL-5水平显著高于慢性鼻炎组和正常组 (P <0 0 1 ) ;而IFN -γ水平却显著低于后两组(P <0 .0 1 )。变应性鼻炎组患者血清的sIL-2R变应性鼻炎组均显著高于后两组 (P <0 .0 1 )且与PBMC培养的上清液中IL -4和IL -5的浓度呈正相关 (r分别为 0 .62 5和 0 .5 95 ,P <0 .0 1 )。与IFN -γ浓度呈负相关(r=-0 .5 80 ,P <0 .0 1 )。结论 :变应性鼻炎患者体内激活的T淋巴细胞是Th2 细胞 ,并释放Th2 细胞因子 ,Th1细胞和Th1细胞因子分泌则受到抑制 ;Th2 Objective:To understand the role of Th 1 and Th 2 cytokines secreted by two different T lymphocytes in allergic rhinitis pathogenesis. Method:The levels of IL-4?IL-5 and IFN-γ in the supernatants of PHA stimulated peripheral blood mononuclear cells (PBMC) as well as sIL-2R and total IgE in the serum were measured by enzyme linked immunosorbent assay(ELISA) in 40 patients with allergic rhinitis,20 patients with chronic nonallergic rhinitis and 20 normal controls.Result:(1) In allergic rhinitis group,the levels of IL-4?IL-5 and sIL-2R were significantly higher than those in chronic nonallergic rhinitis and normal groups (P<0.05) ,but IFN-γ obviously lower than that in other groups.No difference was observed between the chronic nonallergic rhinitis and normal controls ( P>0.05 );(2)sIL-2R was showed positive correlations with IL-4 and IL-5 respectively while a negative correlation with IFN-γ ( P <0.05) . Conclusion:For allergic rhinitis patients,Th 2 cytokines are enhanced while Th 1 cytokines are inhibited.Th 2 cytokines can improve the production of IgE and infiltration of eosinopholia.
出处 《山东医大基础医学院学报》 2002年第3期144-146,共3页
关键词 鼻炎 应变性 常年性 单核白细胞 细胞活素类 白细胞介素4 白细胞介素5 干扰素Ⅱ型 受体 白细胞介素2 Rhinitis,allergic,perennial Leukocytes,mononuclear Interleukin-4 Interleukin-5 Interferon type Ⅱ Receptor,interleukin-2
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