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: Regulation of adaptive immunity by innate immune cells is widely accepted . Conversely , adaptive immune cells can also regulate cells of the innate immune system . Here , we report for the first time the essential role of B cells in regulating macrophage ( MÏ ) phenotype . In vitro B cell/MÏ co-culture experiments together with experiments in transgenic mice models for B-cell deficiency or overexpression showed B1 cells to polarize MÏ to a distinct phenotype . This was characterized by downregulated TNF-Î± , IL-1Î² and CCL3 , but upregulated IL-10 upon LPS stimulation ; constitutive expression of M2 MÏ markers ( e.g . Ym1 , Fizz1 ) and overexpression of TRIF-dependent cytokines ( IFN-Î² , CCL5 ) . Mechanistically , this phenotype was linked to a defective NF-ÎºB activation , but a functional TRIF/STAT1 pathway . B1-cell-derived IL-10 was found to be instrumental in the polarization of these MÏ . Finally , in vivo relevance of B1-cell-induced MÏ polarization was confirmed using the B16 melanoma tumor model where adoptive transfer of B1 cells induced an M2 polarization of tumor-associated MÏ . Collectively , our results define a new mechanism of MÏ polarization wherein B1 cells play a key role in driving MÏ to a unique , but M2-biased phenotype . Future studies along these lines may lead to targeting of B1 cells to regulate MÏ response in inflammation and cancer .
    OUTPUT:

agent
tumor promoting inflammation
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: Regulation of adaptive immunity by innate immune cells is widely accepted . Conversely , adaptive immune cells can also regulate cells of the innate immune system . Here , we report for the first time the essential role of B cells in regulating macrophage ( MÏ ) phenotype . In vitro B cell/MÏ co-culture experiments together with experiments in transgenic mice models for B-cell deficiency or overexpression showed B1 cells to polarize MÏ to a distinct phenotype . This was characterized by downregulated TNF-Î± , IL-1Î² and CCL3 , but upregulated IL-10 upon LPS stimulation ; constitutive expression of M2 MÏ markers ( e.g . Ym1 , Fizz1 ) and overexpression of TRIF-dependent cytokines ( IFN-Î² , CCL5 ) . Mechanistically , this phenotype was linked to a defective NF-ÎºB activation , but a functional TRIF/STAT1 pathway . B1-cell-derived IL-10 was found to be instrumental in the polarization of these MÏ . Finally , in vivo relevance of B1-cell-induced MÏ polarization was confirmed using the B16 melanoma tumor model where adoptive transfer of B1 cells induced an M2 polarization of tumor-associated MÏ . Collectively , our results define a new mechanism of MÏ polarization wherein B1 cells play a key role in driving MÏ to a unique , but M2-biased phenotype . Future studies along these lines may lead to targeting of B1 cells to regulate MÏ response in inflammation and cancer .
    OUTPUT:
