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目的比较高危型人乳头状瘤病毒(HPV)持续性感染所致不同程度的宫颈病变,分析T辅助细胞(Th)在此演变过程中的作用,明确抗HPV感染免疫应答和抗病毒细胞因子在疾病转归中的重要调节机制。方法对86例高危型HPV16/18阳性的患者依所致宫颈病变的不同分为5组,CIN I、CIN II、CIN III,宫颈癌和宫颈炎,检测其INF-γ、TNF-α、IL-10、IL-5、IL-4、IL-2水平,采用方差分析和多元线性回归,分析不同病变患者6种细胞因子的水平差异,及其每个细胞因子对病变程度的影响。结果在宫颈炎、CIN I、CIN II表现为Th 1优势,CIN III和宫颈癌表现为Th 2优势;宫颈炎、CIN I病变组,IL-2、INF-γ、TNF-α均有升高,CIN II仅有IL-2升高。比较回归方程中的标准偏回归系数,对宫颈病变影响程度依次为INF-γ>TNF-α>IL-2>IL-10。结论在抗HPV持续感染免疫应答中,Th 1优势更利于机体清除病毒,Th1向Th2的偏移,可加重宫颈病变。细胞因子对该过程有重要的调节作用,一方面上调或下调免疫反应,增强或抑制免疫应答,另一方面直接作为抗病毒的效应分子发挥作用。
Objective To compare the effects of persistent infection of high-risk human papillomavirus (HPV) on cervical lesions and to analyze the role of T-helper cells (Th) in this evolutionary process. To clarify the effects of anti-HPV infection and anti-viral cytokines Important Regulatory Mechanisms in Disease Outcomes. Methods Totally 86 high-risk HPV16 / 18 positive patients were divided into 5 groups according to their cervical lesions, CIN I, CIN II, CIN III, cervical cancer and cervicitis. The levels of INF-γ, TNF-α, IL The levels of IL-6, IL-10, IL-5, IL-4 and IL-2 were determined by ANOVA and multivariate linear regression respectively. The levels of six cytokines and the effects of each cytokine on the pathological changes were analyzed. Results In cervicitis, CIN I and CIN II showed Th 1 predominance, CIN III and cervical cancer showed Th 2 predominance. Cervicitis, CIN I lesion, IL-2, INF-γ and TNF-α all increased , CIN II only IL-2 increased. Compared with the standard partial regression coefficients in the regression equation, the effects on cervical lesions were INF-γ> TNF-α> IL-2> IL-10. Conclusion Th1 advantage is more beneficial to the clearance of virus in the body when the immune response to HPV persists, and the shift of Th1 to Th2 may aggravate cervical lesions. Cytokines play an important regulatory role in this process. On the one hand, the immune response is up-regulated or down-regulated, and the immune response is enhanced or suppressed. On the other hand, cytokines play a direct role as antiviral effector molecules.