Regulation of Antitumor Immune Responses by the IL‐12 Family Cytokines, IL‐12, IL‐23, and IL‐27
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- Toshinori Nakayama
- editor
書誌事項
- 公開日
- 2010-01
- 権利情報
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- http://creativecommons.org/licenses/by/3.0/
- DOI
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- 10.1155/2010/832454
- 公開者
- Wiley
この論文をさがす
説明
<jats:p>The interleukin (IL)‐12 family, which is composed of heterodimeric cytokines including IL‐12, IL‐23, and IL‐27, is produced by antigen‐presenting cells such as macrophages and dendritic cells and plays critical roles in the regulation of helper T (Th) cell differentiation. IL‐12 induces IFN‐<jats:italic>γ</jats:italic> production by NK and T cells and differentiation to Th1 cells. IL‐23 induces IL‐17 production by memory T cells and expands and maintains inflammatory Th17 cells. IL‐27 induces the early Th1 differentiation and generation of IL‐10‐producing regulatory T cells. In addition, these cytokines induce distinct immune responses to tumors. IL‐12 activates signal transducers and activator of transcription (STAT)4 and enhances antitumor cellular immunity through interferon (IFN)‐<jats:italic>γ</jats:italic> production. IL‐27 activates STAT1, as does IFN‐<jats:italic>γ</jats:italic> and STAT3 as well, and enhances antitumor immunity by augmenting cellular and humoral immunities. In contrast, although exogenously overexpressed IL‐23 enhances antitumor immunity via memory T cells, endogenous IL‐23 promotes protumor immunity through STAT3 activation by inducing inflammatory responses including IL‐17 production.</jats:p>
収録刊行物
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- Journal of Immunology Research
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Journal of Immunology Research 2010 (1), 2010-01
Wiley