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| 1 | Immunobiology of hepatocarcinogenesis: Ways to go or almost there?显示文摘Hepatocellular carcinoma is on the rise and occurs in the setting of chronic liver disease and cirrhosis.Though treatment modalities are available,mortality from this cancer remains high.Medical therapy with the utilization of biologic compounds such as the Food and Drug Administration approved sorafenib might be the only option that can increase survival.Immunotherapy,with modern pharmacologic developments,is a new frontier in cancer therapy and therefore the immunobiology of hepatocarcinogenesis is under investigation.This review will discuss current concepts of immunobiology in hepatocarcinogenesis along with current treatment modalities employing immunotherapy.The tumor microenvironment along with a variety of immune cells coexists and interplays to lead to tumorigenesis.Tumor infiltrating lymphocytes including CD8+ T cells,CD4+ T cells along with regulatory T cells,tumor associated macrophages,tumor associated neutrophils,myeloid derived suppressor cells,and natural killer cells interact to actively provide anti-tumor or pro-tumor effects.Furthermore,oncogenic pathways such as Raf/mitogenactivated protein kinase/extracellular-signal-regulated kinase pathway,phosphatidyl-3-kinase/AKT/mammalian target or rapamycin,Wnt/β-catenin,nuclear factor-κB and signal transducers and activators of transcription 3 may lead to activation and proliferation of tumor cells and are also considered cornerstones in tumorigenesis.Immunotherapy directed at this complex milieu of cells has been showned to be successful in cancer treatment.The use of vaccines,adoptive cell therapy and immune checkpoint inhibitor modulation are current options for therapy.Further translational research will shed light to concepts such as anti-tumor immunity which can add another alternative in the therapeutic armamentarium. | Pavan Patel Steven E Schutzer Nikolaos Pyrsopoulos | 2016 | World Journal of Gastrointestinal Pathophysiology2016，7，3： | 3 |
| 2 | IFN-α治疗对慢性丙型肝炎患者CD8^+T细胞亚群Tim-3表达水平的影响显示文摘为探讨应用IFN-α治疗和未治疗的慢性丙型肝炎患者外周血CD8+T细胞亚群细胞频数及各亚群上Tim-3表达的变化。采用流式细胞术检测IFN-α治疗和未治疗的慢丙肝患者外周血中CD8+T细胞及各亚群频数及膜表面Tim-3表达水平的方法;q T-PCR检测血清中HCV-RNA水平;Spearman相关性分析CD8+T细胞频数、Tim-3表达与HCV-RNA之间的相关性。结果显示,慢丙肝患者外周血CD8+T细胞频数较健康对照组、IFN-α治疗组显著降低(P<0.01)。初始T细胞明显增加(P<0.01)。TCM、TEM细胞分布频率降低(P<0.01)。经IFN-α治疗后,CD8+T细胞百分率上升(P<0.05),初始T细胞数量下降(P<0.01),TCM、TEM细胞频数均升高(P<0.01)。三组人群TEMRA细胞频数无统计学差异。与健康对照组、IFN-α治疗组相比,慢丙肝患者CD8+T细胞及各亚群Tim-3表达水平均有上调(P<0.05)。经抗病毒治疗后,CD8+T细胞、Naive细胞、TEM细胞、TEMRA细胞亚群Tim-3表达明显降低(P<0.05),TCM细胞亚群中Tim-3表达也有降低,但无统计学差异。Spearman相关性分析发现:慢丙肝患者外周血CD8+T细胞百分率与病毒载量呈反比(r=-0.3775,P<0.01),而Tim-3表达水平与病毒载量正相关(r=0.6230,P<0.0001)。由此可知,HCV感染慢性化时可出现CD8+T细胞亚群分布异常及各亚群Tim-3过表达。IFN-α通过调节各CD8+T细胞亚群分化状态,及下调各群细胞表面Tim-3的表达,促进HCV免疫清除。 | 李冰洁 何瑜 贾战生 左维泽 | 2015 | 石河子大学学报(自然科学版)2015，33，3： | 2 |
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