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Potential Immune Escape Mechanisms of Tumors: MHC Class I Molecules – Enemies or Friends

机译:肿瘤的潜在免疫逃生机制:MHC I类分子 - 敌人或朋友

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It is generally accepted that tumor development is a multifactorial process which is caused by a sequential accumulation of different genetic alterations leading to aberrant cell cycle control, instability of genomic integrity as well as decrased recognition by the immune system. During the last decade, the tumor-host interaction has been well defined. It has been demonstrated that professional antigen presenting cells (APC), macrophages, natural killer (NK) cells, NKT cells and in particular T-lymphocytes play a key role in anti-tumor immunity. In general, immune cells monitor MHC class I-presented antigenic peptides. Presentation of self peptides by MHC class I molecules results in the generation of tolerance. In contrast, presentation of viral or tumor-derived foreign antigens leads to the induction of lysis by CD8+ cytotoxic T lymphocytes (CTL).
机译:通常可接受肿瘤发育是多因素过程,该过程是由不同遗传改变的顺序积累导致异常细胞周期控制,基因组完整性的不稳定性以及免疫系统的识别。在过去十年中,肿瘤宿主相互作用已经很好地定义。已经证明,专业抗原呈递细胞(APC),巨噬细胞,天然杀伤(NK)细胞,NKT细胞和特别是T淋巴细胞在抗肿瘤免疫中起关键作用。通常,免疫细胞监测MHC I类呈抗原肽。 MHC I类分子的自肽呈现导致耐受的产生。相反,病毒或肿瘤衍生的外来抗原的呈递导致CD8 +细胞毒性T淋巴细胞(CTL)的裂解诱导。

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