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BCAP Regulates Dendritic Cell Maturation Through the Dual-Regulation of NF-kappa B and PI3K/AKT Signaling During Infection

  1. Author:
    Miao, Yuhui
    Jiang, Ming
    Qi, Lu
    Yang,De
    Xiao, Weihua
    Fang, Fang

  2. Author Address

    Univ Sci & Technol China, Affiliated Hosp 1, Dept Med Oncol, Div Life Sci & Med, Hefei, Peoples R China.Univ Sci & Technol China, Sch Life Sci, CAS Key Lab Innate Immun & Chron Dis, Hefei Natl Lab Phys Sci Microscale, Hefei, Peoples R China.Univ Sci & Technol China, Inst Immunol, Hefei, Peoples R China.Univ Sci & Technol China, Engn Technol Res Ctr Biotechnol Drugs Anhui, Hefei, Peoples R China.NCI, Canc & Inflammat Program, Frederick Natl Lab Canc Res, Ctr Canc Res, Frederick, MD 21701 USA.
    1. Year: 2020
    2. Date: Feb 18
  2. Journal: FRONTIERS IN IMMUNOLOGY
  3. FRONTIERS MEDIA SA,
    1. 11
  5. Type of Article: Article
  6. Article Number: 250
  7. ISSN: 1664-3224
  1. Abstract:

    The maturation of dendritic cells (DCs) is essential in adaptive immunity. B cell adapter for phosphoinositide 3-kinase (BCAP) has been shown a divergent activities in cell type dependent manner including B cells, NK cells, macrophages, and plasmacytoid DCs (pDCs), however, its role in conventional DCs (cDCs) remains unknown. Here, we report that BCAP negatively regulates Toll-like receptor-induced cDC maturation and inhibits cDCs from inducing antigen-specific T cell responses, thereby weakening the antibacterial adaptive immune responses of mice in a Listeria monocytogenes-infection model. Furthermore, we demonstrate that BCAP simultaneously modulates the activation of the NF-kappa B and PI3K/AKT signaling by dynamically interacting with, respectively, MyD88 and the p85 alpha subunit of PI3K. Our study thus reveals non-redundant roles for BCAP in regulating cDC maturation and reveals a bilateral signal transduction mechanism.

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External Sources

  1. View Full Text
  2. DOI: 10.3389/fimmu.2020.00250
  3. PMID: 32133012
  4. PMCID: PMC7040100
  5. View record in Web of Science®
  6. WOS: 000518610200001

Library Notes

  1. Fiscal Year: FY2019-2020
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