Ginsenoside compound-K inhibits the activity of B cells through inducing IgD-B cell receptor endocytosis in mice with collagen-induced arthritis

Mei Zhang, Shanshan Hu, Juan Tao, Weijie Zhou, Rui Wang, Yu Tai, Feng Xiao, Qingtong Wang, Wei Wei

Research output: Contribution to journalArticle

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Abstract

Previously, ginsenoside metabolite compound K (C-K) was able to reduce B cell proliferation and serum anti-type II collagen (anti-CII) antibody to normal levels in mice with collagen-induced arthritis (CIA); however, the mechanism by which C-K restores B cell balance is unclear. In the present work, C-K treatment not only alleviated the polyarthritis index, swollen joint count, pathological scores of spleen and joints, spleen index, B cell proliferation and the level of serum antibodies (IgG1, IgG2a and anti-collagen II), but C-K treatment also restored B cell subsets including regulatory B cells, plasma cells, memory B cells, mature B cells, and follicular B cells in CIA mice. Interestingly, C-K did not change the expression level of immunoglobulin D-type B-cell receptor (IgD-BCR) but promoted IgD-BCR endocytosis. C-K treatment enhanced β-arrestin1 expression, facilitating the colocalization between IgD and β-arrestin1, as well as colocalization between IgD and adaptor protein 2 (AP2). Inhibition of the β-arrestin1-AP2 interaction with barbadin significantly reduced the ability of C-K to attenuate IgD-BCR plasma membrane localization. These results taken together depict that C-K ameliorates CIA in part by inhibiting B cell activation through the triggering of IgD-BCR internalization in a β-arrestin1-AP2 dependent manner.

Original languageEnglish (US)
JournalInflammopharmacology
DOIs
StatePublished - Jan 1 2019
Externally publishedYes

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Keywords

  • B cell
  • Collagen-induced arthritis
  • Endocytosis
  • Ginsenoside compound K
  • β-arrestin1

ASJC Scopus subject areas

  • Immunology
  • Pharmacology
  • Pharmacology (medical)

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