Tumor immune escape by immunoregulatory CD4 T cells

癌症免疫监测理论已经被广泛接受，但科学基础仍然是模糊的。肿瘤免疫逃逸也是一个关于任何机制的理论，它并不完全过时。最近，通过宿主免疫系统识别的肿瘤抗原已在分子水平上识别，以及对肿瘤免疫学的肿瘤免疫反应的分析，免疫监测的理论和肿瘤免疫逃逸应该被谨慎地重新评价。在本研究中，使用BALB/c辐射白血病RL 1关于我们以前在哪里已经识别的特异性肽识别的特异CTL作为模型肿瘤，我们已识别的肿瘤或抗原特异性调节CD 4 T细胞。We showed that altered Akt molecule which is dominant antigen in RL？1刺激免疫抑制因子CD4T cells and inhibited efficient generation of CD8CTL which recognized the tumor antigen peptide derived also from the Akt molecule.Beside those tumor antigen specific regulatory CD4T cells， we also found immunoregulatory CD4イD1+イD1T cells which were tumor antigen non-specific.这些细胞是由自动抗原激活的，并受自动免疫保护。We showed that by in vivo depletion of CD4イイD1+イエD1 CD25イイD1+イエD1 T cells， efficient tumor rejection res隅occurred。

Cancer immune surveillance theory has been widely accepted, but the scientific basis is still obscure. Tumor immune escape is also a theory of which mechanisms have not fully elucidated. Recently, tumor antigens recognized by the host immune system have been identified at molecular level, and the analysis of tumor immune responses against the tumor immunology, theories of the immune surveillance and the tumor immune escape should be carefully reevaluated.In this study, using BALB/c radiation leukemia RL♂1 on which we previously identified the antigen peptide recognized by the specific CTL as a model tumor, we identified tumor antigen specific regulatory CD4 T cells. We showed that altered Akt molecule which is dominant antigen in RL♂1 stimulated immunoregulatory CD4 T cells and inhibited efficient generation of CD8 CTL which recognized the tumor antigen peptide derived also from the Akt molecule.Beside those tumor antigen specific regulatory CD4 T cells, we also found immunoregulatory CD4ィイD1+ィエD1CD25ィイD1+ィエD1 T cells which were tumor antigen non-specific. Those cells were activated by autoantigens and protected from auto immunity. We showed that by in vivo depletion of CD4ィイD1+ィエD1CD25ィイD1+ィエD1 T cells, efficient tumor rejection response occurred.