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宫颈癌是危害全世界妇女健康的主要恶性肿瘤之一。宫颈癌及其癌前病变——鳞状上皮内病变(SIL)均由高危型人乳头瘤病毒(HPV)持续感染导致。HPV通过下调干扰素表达,促进白介素(IL)-10和转化生长因子(TGF)-β1表达,产生局部免疫抑制微环境,改变肿瘤表面抗原,抑制肿瘤免疫应答。本研究从分子水平分析论述肿瘤微环境中HPV和宫颈癌细胞通过可溶性免疫抑制因子IL-10、TGF-β1逃避宿主免疫反应可能的机制,阐明IL-10、TGF-β1在HPV感染中的免疫抑制功能。
Cervical cancer is one of the major malignancies that endanger the health of women throughout the world. Cervical cancer and its precancerous lesions - squamous intraepithelial lesion (SIL) are caused by the continuous infection of high-risk human papillomavirus (HPV). HPV can downregulate the expression of interferon, promote the expression of interleukin (IL) -10 and transforming growth factor (TGF) -β1, produce local immunosuppressive microenvironment, alter tumor surface antigens and inhibit tumor immune response. In this study, molecular level analysis of HPV and cervical cancer cells in tumor microenvironment by soluble immunosuppressive factors IL-10, TGF-β1 escape the possible mechanism of host immune response to clarify the IL-10, TGF-β1 immunity in HPV infection Suppression function.