C-type lectin receptor Dectin-2 binds to an endogenous protein β-glucuronidase on dendritic cells

Daiki Mori, Kensuke Shibata, Sho Yamasaki

    Research output: Contribution to journalArticle

    7 Citations (Scopus)

    Abstract

    C-type lectin receptors (CLRs) recognize pathogen-derived ligands and abnormal self that trigger protective immune responses. However, the precise nature of self ligands recognized by CLRs remains to be determined. Here, we found that Dectin-2 recognizes bone marrow-derived dendritic cells (BMDCs) using Dectin-2-expressing reporter cells. This activity was inhibited by an excessive amount of mannose, and by the mutation of mannose-binding motif in Dectin-2. β-glucuronidase (Gusb) was identified as a protein bound to Dectin-2 and mutations of N-glycosylation sites in Gusb impaired the binding of Gusb to Dectin-2. Overexpression of Gusb in a macrophage cell line conferred an ability to stimulate Dectin-2-expressing reporter cells. Our study suggests that a glycosylated protein with mannose-related structure is recognized by Dectin-2.

    Original languageEnglish
    Article numbere0169562
    JournalPloS one
    Volume12
    Issue number1
    DOIs
    Publication statusPublished - Jan 2017

    All Science Journal Classification (ASJC) codes

    • Biochemistry, Genetics and Molecular Biology(all)
    • Agricultural and Biological Sciences(all)
    • General

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