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TAGAP instructs Th17 differentiation by bridging Dectin activation to EPHB2 signaling in innate antifungal response

Author

Listed:
  • Jianwen Chen

    (Huazhong University of Science and Technology)

  • Ruirui He

    (Huazhong University of Science and Technology)

  • Wanwei Sun

    (Huazhong University of Science and Technology)

  • Ru Gao

    (Huazhong University of Science and Technology)

  • Qianwen Peng

    (Huazhong University of Science and Technology)

  • Liwen Zhu

    (Nanjing University)

  • Yanyun Du

    (Huazhong University of Science and Technology)

  • Xiaojian Ma

    (Huazhong University of Science and Technology)

  • Xiaoli Guo

    (Huazhong University of Science and Technology)

  • Huazhi Zhang

    (Huazhong University of Science and Technology)

  • Chengcheng Tan

    (Huazhong University of Science and Technology)

  • Junhan Wang

    (University-Affiliated Hospital, Huazhong University of Science and Technology)

  • Wei Zhang

    (Huazhong University of Science and Technology)

  • Xiufang Weng

    (Huazhong University of Science and Technology)

  • Jianghong Man

    (National Center of Biomedical Analysis)

  • Hermann Bauer

    (Max Planck Institute for Molecular Genetics)

  • Qing K. Wang

    (Huazhong University of Science and Technology
    Cleveland Clinic Lerner College of Medicine of Case Western Reserve University
    Cleveland Clinic Lerner College of Medicine of Case Western Reserve University)

  • Bradley N. Martin

    (Harvard Medical School)

  • Cun-Jin Zhang

    (Nanjing University)

  • Xiaoxia Li

    (Department of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic)

  • Chenhui Wang

    (Huazhong University of Science and Technology
    Wuhan Institute of Biotechnology)

Abstract

The TAGAP gene locus has been linked to several infectious diseases or autoimmune diseases, including candidemia and multiple sclerosis. While previous studies have described a role of TAGAP in T cells, much less is known about its function in other cell types. Here we report that TAGAP is required for Dectin-induced anti-fungal signaling and proinflammatory cytokine production in myeloid cells. Following stimulation with Dectin ligands, TAGAP is phosphorylated by EPHB2 at tyrosine 310, which bridges proximal Dectin-induced EPHB2 activity to downstream CARD9-mediated signaling pathways. During Candida albicans infection, mice lacking TAGAP mount defective immune responses, impaired Th17 cell differentiation, and higher fungal burden. Similarly, in experimental autoimmune encephalomyelitis model of multiple sclerosis, TAGAP deficient mice develop significantly attenuated disease. In summary, we report that TAGAP plays an important role in linking Dectin-induced signaling to the promotion of effective T helper cell immune responses, during both anti-fungal host defense and autoimmunity.

Suggested Citation

  • Jianwen Chen & Ruirui He & Wanwei Sun & Ru Gao & Qianwen Peng & Liwen Zhu & Yanyun Du & Xiaojian Ma & Xiaoli Guo & Huazhi Zhang & Chengcheng Tan & Junhan Wang & Wei Zhang & Xiufang Weng & Jianghong Ma, 2020. "TAGAP instructs Th17 differentiation by bridging Dectin activation to EPHB2 signaling in innate antifungal response," Nature Communications, Nature, vol. 11(1), pages 1-16, December.
    • Handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-15564-7
    DOI: 10.1038/s41467-020-15564-7
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