Ginsenoside compound K suppresses the abnormal activation of T lymphocytes in mice with collagen-induced arthritis

Abstract

C-K suppresses the progression of CIA through regulating TCR, CD28, CTLA-4 and PD-1 expression, thus inhibiting the abnormal activation and differentiation of T lymphocytes.

Ginsenoside metabolite compound K exerts anti-inflammatory effect via suppressing T cell activation

“…Our recent study demonstrated that the expression of CD80, CD86, and MHCII on DCs were inhibited by CK. Consistent with this result, CK decreased the expression of TCR, CD28 and CD25 on T cells [11,12] , and suppressed IL-2 secretion from T cells [11] . These results suggest that the effect of CK on suppressing T cell activation may be due to reducing the signals provided by DCs.…”

“…In our previous studies, it has been reported that CK up-regulated the percentages of Tregs in CIA mice [12] . The pivotal role of Tregs in autoimmune diseases such as RA has been established [33] .…”

“…Biological agents inhibiting T cells activation has been identified efficacy in the treatment of autoimmune disease including RA [18,19] . Our previous studies showed that CK reduced inflammatory cytokine levels including IL-1β, TNF-α, IL-2, and IL-17 [11,12,20] . In addition, CK decreased activated T-cells, and raised naive T-cells and Treg cells in spleen [11,12] , reduced expression of T cell receptor (TCR), CD28, and CD25 on T cells [11,12,20] .…”

“…Our previous studies showed that CK attenuated adjuvant-induced arthritis (AA) and collagen-induced arthritis (CIA) by suppressing T cell activation [10][11][12] . Our understanding of the immunopathology of autoimmune disease has been improved by recent progress in the research of T cells.…”

The ginsenoside metabolite compound K exerts its anti-inflammatory activity by downregulating memory B cell in adjuvant-induced arthritis

“…CK also exerts anti-inflammatory effects by inhibiting cyclooxygenase-2 expression (Park et al, 2005). Our previous work demonstrated that CK attenuated arthritis in animal models by suppressing T cell activation, inhibiting the production of inflammatory cytokines such as IL-1b, tumor necrosis factor-alpha (TNF-a), IL-2, and IL-17, inhibiting the proliferation of B cells, and decreasing autoantibody levels (Chen et al, 2014;Liu et al, 2014;Wu et al, 2014). However, its effect and mechanism of action on memory B cells remains unclear.…”