TNF-α enhances Th9 cell differentiation and antitumor immunity via TNFR2-dependent pathways View Full Text


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Article Info

DATE

2019-12

AUTHORS

Yuxue Jiang, Jintong Chen, Enguang Bi, Yinghua Zhao, Tianxue Qin, Yiming Wang, Alison Wang, Sujun Gao, Qing Yi, Siqing Wang

ABSTRACT

Tumor specific Th9 cells are potential effector cells for adoptive therapy of human cancers. TNF family members OX40L, TL1A and GITRL have been shown to promote the induction of Th9 cells and antitumor immunity. However, the role of TNF-α, the prototype of the TNF superfamily cytokines, in Th9 cell differentiation and their antitumor efficacy is not defined. Here, we showed that TNF-α potently promoted naïve CD4+ T cells to differentiate into Th9 cells in vitro. Furthermore, the addition of TNF-α during Th9 cell differentiation increased T cell survival and proliferation. More importantly, the adoptive transfer of TNF-α-treated Th9 cells induced more potent antitumor effects than regular Th9 cells in mouse tumor model. TNF-α signals via two cell surface receptors, TNFR1 and TNFR2. Mechanistic studies revealed that TNF-α drove Th9 cell differentiation through TNFR2 but not TNFR1. In addition, under Th9 polarizing condition, TNF-α activated STAT5 and NF-κB pathways in T cells in a TNFR2-dependent manner. Inhibition of STAT5 and NF-κB pathways by their specific inhibitors impaired TNF-α-induced Th9 cell differentiation. Our results identified TNF-α as a new powerful inducer of Th9 cells and clarified the molecular mechanisms underlying TNF-α-induced Th9 cell differentiation. More... »

PAGES

28

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1186/s40425-018-0494-8

    DOI

    http://dx.doi.org/10.1186/s40425-018-0494-8

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1111916529

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30717817


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        "description": "Tumor specific Th9 cells are potential effector cells for adoptive therapy of human cancers. TNF family members OX40L, TL1A and GITRL have been shown to promote the induction of Th9 cells and antitumor immunity. However, the role of TNF-\u03b1, the prototype of the TNF superfamily cytokines, in Th9 cell differentiation and their antitumor efficacy is not defined. Here, we showed that TNF-\u03b1 potently promoted na\u00efve CD4+ T cells to differentiate into Th9 cells in vitro. Furthermore, the addition of TNF-\u03b1 during Th9 cell differentiation increased T cell survival and proliferation. More importantly, the adoptive transfer of TNF-\u03b1-treated Th9 cells induced more potent antitumor effects than regular Th9 cells in mouse tumor model. TNF-\u03b1 signals via two cell surface receptors, TNFR1 and TNFR2. Mechanistic studies revealed that TNF-\u03b1 drove Th9 cell differentiation through TNFR2 but not TNFR1. In addition, under Th9 polarizing condition, TNF-\u03b1 activated STAT5 and NF-\u03baB pathways in T cells in a TNFR2-dependent manner. Inhibition of STAT5 and NF-\u03baB pathways by their specific inhibitors impaired TNF-\u03b1-induced Th9 cell differentiation. Our results identified TNF-\u03b1 as a new powerful inducer of Th9 cells and clarified the molecular mechanisms underlying TNF-\u03b1-induced Th9 cell differentiation.", 
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    RDF/XML is a standard XML format for linked data.

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