human
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
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    INPUT: Evaluation of immune dysfunction during the tumor-bearing state is a critical issue in combating cancer . In this study , we initially found that IL-6 , one of the cachectic factors , suppressed CD4(+) T cell-mediated immunity through downregulation of MHC class II by enhanced arginase activity of dendritic cells ( DC ) in tumor-bearing mice . We demonstrated that administration of Ab against IL-6R ( anti-IL-6R mAb ) greatly enhanced T cell responses and inhibited the growth of tumor in vivo . We also found that IL-6 upregulated the expression of arginase-1 and arginase activity of DC in vitro . Tumor-infiltrating CD11c(+) DC exhibited upregulated mRNA expression of arginase-1 but reduced expression of MHC class II in parallel with the increase in serum IL-6 levels at the late stage in tumor-bearing hosts . However , the administration of anti-IL-6R mAb into tumor-bearing mice inhibited both the downmodulation of MHC class II and the upregulation of arginase-1 mRNA levels in DC . Furthermore , we noted that N(Ï)-hydroxy-L-arginine or L-arginine , an arginase-1 inhibitor , blocked the reduction in MHC class II levels on CD11c(+) DC during the tumor-bearing state . Finally , we demonstrated that the administration of N(Ï)-hydroxy-L-arginine at the peritumor site significantly enhanced CD4(+) T cell responses and inhibited tumor growth . Thus , IL-6-mediated arginase activation and the subsequent reduction in MHC class II expression on DC appeared to be critical mechanisms for inducing dysfunction of the immune system in the tumor-bearing state . Blockade of the IL-6-arginase cascade is a promising tool to overcome the dysfunction of antitumor immunity in tumor-bearing hosts .
    OUTPUT:

agent
avoiding immune destruction
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
    ###
    INPUT: Evaluation of immune dysfunction during the tumor-bearing state is a critical issue in combating cancer . In this study , we initially found that IL-6 , one of the cachectic factors , suppressed CD4(+) T cell-mediated immunity through downregulation of MHC class II by enhanced arginase activity of dendritic cells ( DC ) in tumor-bearing mice . We demonstrated that administration of Ab against IL-6R ( anti-IL-6R mAb ) greatly enhanced T cell responses and inhibited the growth of tumor in vivo . We also found that IL-6 upregulated the expression of arginase-1 and arginase activity of DC in vitro . Tumor-infiltrating CD11c(+) DC exhibited upregulated mRNA expression of arginase-1 but reduced expression of MHC class II in parallel with the increase in serum IL-6 levels at the late stage in tumor-bearing hosts . However , the administration of anti-IL-6R mAb into tumor-bearing mice inhibited both the downmodulation of MHC class II and the upregulation of arginase-1 mRNA levels in DC . Furthermore , we noted that N(Ï)-hydroxy-L-arginine or L-arginine , an arginase-1 inhibitor , blocked the reduction in MHC class II levels on CD11c(+) DC during the tumor-bearing state . Finally , we demonstrated that the administration of N(Ï)-hydroxy-L-arginine at the peritumor site significantly enhanced CD4(+) T cell responses and inhibited tumor growth . Thus , IL-6-mediated arginase activation and the subsequent reduction in MHC class II expression on DC appeared to be critical mechanisms for inducing dysfunction of the immune system in the tumor-bearing state . Blockade of the IL-6-arginase cascade is a promising tool to overcome the dysfunction of antitumor immunity in tumor-bearing hosts .
    OUTPUT:
