Ethyl Caffeate Ameliorates Collagen-Induced Arthritis by Suppressing Th1 Immune Response

The present study was designed to assess the antiarthritic potential of ecf in collagen-induced arthritis (cia) and explore its underlying mechanism. methods. in vitro,lymphocyte proliferation assay was measured by cck-8 kit. in vivo,the therapeutic potential of ecf on cia was investigated; surface marker,treg cell,and intracellular cytokines (il-17a and ifn-γ) were detected by flow cytometry. th1 cell differentiation assay was performed,and mrna expression in interferon-γ-related signaling was examined by q-pcr analysis. results. in vitro,ecf markedly inhibited the proliferation of splenocytes in response to cona and anti-cd3. in vivo,ecf treatment reduced the severity of cia,inhibited ifn-γ and il-6 secretion,and decreased the proportion of cd11b+gr-1+ splenic neutrophil. meanwhile,ecf treatment significantly inhibited the ifn-γ expression in cd4+t cell without obviously influencing the development of th17 cells and t regulatory cells. in vitro,ecf suppressed the differentiation of naive cd4+ t cells into th1. furthermore,ecf intensely blocked the transcriptional expression in interferon-γ-related signaling,including ifn-γ,t-bet,stat1,and stat4. conclusion. our results indicated that ecf exerted antiarthritic potential in collagen-induced arthritis by suppressing th1 immune response and interferon-γ-related signaling. © 2017 shikui xu et al.