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PAX3-FKHR chimeric oncoprotein: hiding itself from immune detection?

机译：PAX3-FKHR嵌合癌蛋白：自身无法进行免疫检测？

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The ability of cancer cells to avoid detection by the immune system has been a subject of debate and controversy since it was initially described in terms of the immune surveillance hypothesis by Burnet and Thomas in the 1950s.Broadly speaking immune surveillance implies the existence of tumor antigens, molecular markers that could serve as a target for the immune system by virtue of their mutation, or overexpression by transcriptional, genetic or epigenetic mechanisms. Naturally occurring tumor antigens have been most frequently and convincingly described in the context of viral infection, and the overexpression of onco-fetal antigens in cancers such as melanoma.Key evidence in favor of immune surveillance is the immunoinhibitory environment of tumors and of cancer patients as exemplified by high circulating levels of immunoinhibitory cytokines such as IL10 and TGFP,loss of MHC class I or P2-microglobulin expression,increase in regulatory T cell numbers and activity,and decrease in numbers and activity of dendritic cells.Arguments against immune surveillance have included the contention that its existence In normal individuals should necessitate an increased incidence of cancer in patients with severe immunodeficiencies. However, within this patient population, apart from specific viral associated malignancies such as EBV driven lymphoproliferative diseases, Hodgkins or Kaposi's sarcoma, there is no significant increase in common cancers.
机译：自从1950年代Burnet和Thomas提出免疫监视假说以来，癌细胞避免被免疫系统检测的能力一直是争论和争议的话题。广义而言，免疫监视隐含着肿瘤抗原的存在。分子标记，由于其突变或转录，遗传或表观遗传机制的过度表达，可以作为免疫系统的靶标。天然存在的肿瘤抗原在病毒感染以及癌基因抗原在诸如黑素瘤等癌症中的表达最为频繁和令人信服。支持免疫监测的关键证据是肿瘤和癌症患者的免疫抑制环境，例如例如，高循环水平的免疫抑制细胞因子（例如IL10和TGFP），I类MHC或P2-微球蛋白的表达减少，调节性T细胞数量和活性增加，树突细胞数量和活性下降。有关其存在的论点是，在正常个体中，严重免疫缺陷患者应增加癌症的发病率。但是，在该患者人群中，除了特定的病毒相关恶性肿瘤（如EBV驱动的淋巴增生性疾病，霍奇金斯病或卡波西氏肉瘤）外，常见癌症没有显着增加。

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