Therapeutic effects of TACI-Ig on rats with adjuvant-induced arthritis via attenuating inflammatory responses

Cao, Yan; Wu, Yujing; Wang, Di; Wei, Wei; Qin, Qiong; Xie, Guoxiong; Zhang, Lingling; Su, Yan; Chen, Jingyu; Wang, Qingtong; Wu, Huaxun; Xiao, Feng; Sun, Wei; Jin, Juan; Wang, Wenxiang

doi:10.1093/rheumatology/keq404

Cited by 62 publications

(40 citation statements)

References 42 publications

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“…Abnormal activation of T cells contributes to the immune damage and synovial pathological histology change in RA [13] . Animal models confirm the role of T cells in chronic inflammatory arthritis [14,15] . A down-regulated percentage of naive T cells, an up-regulated percentage of activated T cells, and abnormal proliferation of T cells were demonstrated in AA and CIA [14][15][16][17] .…”

Section: Research Highlightmentioning

confidence: 76%

“…Animal models confirm the role of T cells in chronic inflammatory arthritis [14,15] . A down-regulated percentage of naive T cells, an up-regulated percentage of activated T cells, and abnormal proliferation of T cells were demonstrated in AA and CIA [14][15][16][17] . Biological agents inhibiting T cells activation has been identified efficacy in the treatment of autoimmune disease including RA [18,19] .…”

Section: Research Highlightmentioning

confidence: 76%

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

2015

Inflamm Cell Signal

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Ginsenoside metabolite compound K (CK) is a metabolite of ginsenoside, and belongs to dammarane-type triterpene saponins according to its structure. It has been reported that CK exerts anti-inflammatory activity. Our previous studies showed that CK alleviated adjuvant-induced arthritis (AA) and collagen-induced arthritis (CIA) via suppressing T cell activation. Our recent study showed that the inhibitory effect of CK on T cell activation was due to suppressing CCL21-CCR7-mediated migration of dendritic cells (DCs) and signals between T cells and DCs. In this brief review, we summarize recent studies on the anti-inflammatory effect of CK and highlight recent advances in our understanding of how CK contributes to the anti-inflammatory effect via suppressing T cell activation in autoimmune conditions. Elucidating the possible mechanism of CK responsible for the anti-inflammatory effect may provide a rationale for development of CK as new therapeutic agents in treatment of inflammatory and autoimmune disease.

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Section: Research Highlightmentioning

confidence: 76%

Section: Research Highlightmentioning

confidence: 76%

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

2015

Inflamm Cell Signal

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“…The excessive activation of T cells causes undesirable immune responses against self-antigens, which then results in chronic inflammatory and autoimmune response (Pablos and Cañete, 2013;Rodeghero et al, 2013). In our previous study, a decreased percentage of naive T cells, a raised percentage of activated T cells, and hyperplasia of T cells were observed in autoimmune arthritis animal models (Chang et al, 2011;Liu et al, 2011;Song et al, 2013;Zhang et al, 2013).…”

Section: Introductionmentioning

confidence: 93%

Ginsenoside Metabolite Compound K Suppresses T-Cell Priming via Modulation of Dendritic Cell Trafficking and Costimulatory Signals, Resulting in Alleviation of Collagen-Induced Arthritis

Chen

Wang

et al. 2015

J Pharmacol Exp Ther

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Ginsenoside metabolite compound K (CK; 20-O-D-glucopyranosyl-20(S)-protopanaxadiol), a novel ginsenoside metabolite, belongs to the dammarane-type triterpene saponins, according to its structure. The anti-inflammatory activity of CK has been identified in several studies. Our study demonstrated that CK exerted an anti-inflammatory effect in collagen-induced arthritis (CIA) and adjuvant-induced arthritis animal models, and this effect was due to inhibition of the abnormal activation and differentiation of T cells. However, the mechanism of CK in suppressing T-cell activation remains unclear. In this study, CK had a therapeutic effect in mice with CIA, decreased the percentage of activated T cells and dendritic cells (DCs), and increased the percentage of naive T cells in lymph nodes. The inhibitory effect on T-cell activation of CK was related to suppression of accumulation of DCs in lymph nodes. CK decreased CCL21 levels in lymph nodes and CCR7 expression in DCs and suppressed CCL21/CCR7-mediated migration of DCs, thus reducing accumulation of DCs in lymph nodes. In addition, signals for T-cell activation including major histocompatibility complex class II and costimulatory molecules, such as CD80 and CD86, were suppressed by CK, and the proliferation of T cells induced by DCs was inhibited by CK. In conclusion, this study demonstrated that CK downregulated DC priming of T-cell activation in CIA, and suppression of CCL21/CCR7-mediated DC migration and signaling between T cells and DCs might be the potential mechanism. These results provide an interesting, novel insight into the potential mechanism by which CK contributes to the anti-inflammatory effect in autoimmune conditions.

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“…111,113 Serum levels of BLyS and APRIL are increased in the serum of patients with Very Early Rheumatoid Arthritis (VERA, disease duration <6 wk) 114 and there are higher levels of APRIL and BLyS in synovial fluid than in matched serum, suggesting local production. 115 A TACI-Ig fusion protein that neutralizes both soluble BLyS and APRIL has demonstrated efficacy in rat adjuvantinduced arthritis 116 while treatment in synovium:SCID chimeras resulted in loss of germinal centers within the transplanted tissue. 117 Synovial immunohistochemistry demonstrates production of BLyS by CD68 + macrophages and APRIL by CD83 + DC.…”

Section: B Cell Cytokinesmentioning

confidence: 99%

Emerging immunotherapies for rheumatoid arthritis

Reynolds

Cooles

Isaacs

et al. 2014

Human Vaccines & Immunotherapeutics

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Therapeutic effects of TACI-Ig on rats with adjuvant-induced arthritis via attenuating inflammatory responses

Abstract: Data presented here demonstrate that administration of TACI-Ig significantly attenuates progression of experimental arthritis, with reductions in inflammatory response and bone and joint destruction.

Cited by 62 publications

References 42 publications

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

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

Ginsenoside Metabolite Compound K Suppresses T-Cell Priming via Modulation of Dendritic Cell Trafficking and Costimulatory Signals, Resulting in Alleviation of Collagen-Induced Arthritis

Emerging immunotherapies for rheumatoid arthritis

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