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

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.

• Authors: Mei Zhang, Shanshan Hu, Juan Tao, Weijie Zhou, Rui Wang, Yu Tai, Feng Xiao, Qingtong Wang, Wei Wei
• Journal: Inflammopharmacology (Inflammopharmacology) Vol. 27 Issue 4 Pg. 845-856 (Aug 2019) ISSN: 1568-5608 [Electronic] Switzerland
• PMID: 31165333 (Publication Type: Journal Article)

Chemical References

• Adaptor Protein Complex 2
• Ginsenosides
• Immunoglobulin D
• Immunoglobulin G
• Receptors, Antigen, B-Cell
• beta-Arrestin 1
• Collagen
• ginsenoside M1

Topics

• Adaptor Protein Complex 2 (metabolism)
• Animals
• Arthritis, Experimental (chemically induced, drug therapy, metabolism)
• B-Lymphocytes (drug effects, metabolism)
• Cell Membrane (drug effects, metabolism)
• Cell Proliferation (drug effects)
• Collagen (pharmacology)
• Endocytosis (drug effects)
• Ginsenosides (pharmacology)
• Immunoglobulin D (metabolism)
• Immunoglobulin G (metabolism)
• Joints (drug effects, metabolism)
• Lymphocyte Activation (drug effects)
• Male
• Mice
• Receptors, Antigen, B-Cell (metabolism)
• Spleen (drug effects, metabolism)
• beta-Arrestin 1 (metabolism)