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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >FOLLICULAR LYMPHOMAS CAN BE INDUCED TO PRESENT ALLOANTIGEN EFFICIENTLY - A CONCEPTUAL MODEL TO IMPROVE THEIR TUMOR IMMUNOGENICITY
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FOLLICULAR LYMPHOMAS CAN BE INDUCED TO PRESENT ALLOANTIGEN EFFICIENTLY - A CONCEPTUAL MODEL TO IMPROVE THEIR TUMOR IMMUNOGENICITY

机译:可以有效地诱导出肺淋巴瘤存在的异源抗原-一种改善其肿瘤免疫原性的概念模型

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摘要

In the tumor-bearing host, T cells invariably fail to induce a clinically significant antitumor immune response, Although model systems support the existence of tumor peptide antigens, the molecular interactions critical for antigen presentation by the tumor cell remain unresolved, Here, we demonstrate that human follicular lymphoma cells are highly inefficient at presenting alloantigen despite their strong expression of major histocompatibility complex and low-to-intermediate expression of some adhesion and B7 costimulatory molecules, Activation of follicular lymphoma cells via CD40 induces or up-regulates both adhesion and B7 costimulatory molecules essential to repair this defect, More importantly, once primed, alloreactive T cells efficiently recognize unstimulated follicular lymphoma cells. Thus, correction of defective tumor immunity requires not only expression of major histocompatibility complex but also sufficient expression of multiple adhesion and costimulatory molecules. [References: 28]
机译:在携带肿瘤的宿主中,T细胞始终无法诱导出具有临床意义的抗肿瘤免疫反应。尽管模型系统支持肿瘤肽抗原的存在,但对于肿瘤细胞抗原呈递至关重要的分子相互作用仍未解决,在这里,我们证明了尽管人类滤泡性淋巴瘤细胞主要组织相容性复合物的强表达以及某些黏附和B7共刺激分子的中低表达,但它们在表达同种抗原方面仍然非常低效。通过CD40激活的滤泡性淋巴瘤细胞诱导或上调黏附和B7共刺激。修复该缺陷必不可少的分子,更重要的是,一旦引发,同种异体反应性T细胞就会有效识别未刺激的滤泡性淋巴瘤细胞。因此,校正不良的肿瘤免疫力不仅需要表达主要的组织相容性复合物,而且还需要充分表达多种粘附和共刺激分子。 [参考:28]

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