title: Jaceosidin inhibits contact hypersensitivity in mice via down-regulating IFN-γ/STAT1/T-bet signaling in T cells.
abstract: In the present study, we aimed to investigate the immunosuppressive activity of jaceosidin, a flavone isolated from Artemisia vestita, on T lymphocytes both in vitro and in vivo, and further explore its potential molecular mechanism. Jaceosidin exerted a significant inhibition on the T cell proliferation and activation induced by concanavalin A (Con A) in a concentration-dependent manner and it also inhibited the secretion of the proinflammatory cytokines such as IL-2, TNF-α and IFN-γ of activated T cells. Further study showed that jaceosidin down-regulated STAT1 activation and T-bet expression in activated T cells. Moreover, in order to investigate the immunosuppressive effect of jaceosidin in vivo, the picryl chloride (PCl)-induced ear contact dermatitis model was performed on BALB/c mice. Jaceosidin significantly ameliorated PCl-induced ear swelling in a dose-dependent manner, which was due to its inhibition of the STAT1/T-bet signaling pathway. In summary, these findings suggest that jaceosidin exerts its immunosuppressive effect both in vitro and in vivo through inhibiting T cell proliferation and activation, which is closely associated with its potent down-regulation of the IFN-γ/STAT1/T-bet signaling pathway.
authors.affiliation: School of Life Sciences, Nanjing University, Nanjing 210093, China.
authors.forename: Ye
authors.initials: Y
authors.lastname: Yin
authors.forename: Yang
authors.initials: Y
authors.lastname: Sun
authors.forename: Liyun
authors.initials: L
authors.lastname: Gu
authors.forename: Wei
authors.initials: W
authors.lastname: Zheng
authors.forename: Fangyuan
authors.initials: F
authors.lastname: Gong
authors.forename: Xingxin
authors.initials: X
authors.lastname: Wu
authors.forename: Yan
authors.initials: Y
authors.lastname: Shen
authors.forename: Qiang
authors.initials: Q
authors.lastname: Xu
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000378:metabolism; D000945:Antigens, Differentiation, T-Lymphocyte / Q000378:metabolism; D049109:Cell Proliferation / Q000187:drug effects; D003208:Concanavalin A / Q000494:pharmacology; D016207:Cytokines / Q000096:biosynthesis; D003877:Dermatitis, Contact / Q000188:drug therapy / Q000276:immunology* / Q000378:metabolism; D015536:Down-Regulation / Q000187:drug effects* / Q000276:immunology; D005260:Female; D005419:Flavonoids / Q000494:pharmacology*; D007166:Immunosuppressive Agents / Q000494:pharmacology; D007371:Interferon-gamma / Q000378:metabolism*; D053645:Interleukin-2 Receptor alpha Subunit / Q000378:metabolism; D037181:Lectins, C-Type / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D050794:STAT1 Transcription Factor / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects / Q000276:immunology; D020825:T-Box Domain Proteins / Q000378:metabolism*; D013601:T-Lymphocytes / Q000166:cytology / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D014302:Trinitrobenzenesulfonic Acid / Q000009:adverse effects; D000098815:T-bet Transcription Factor; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D003208:Concanavalin A; D016207:Cytokines; D005419:Flavonoids; D007166:Immunosuppressive Agents; D007371:Interferon-gamma; D053645:Interleukin-2 Receptor alpha Subunit; D037181:Lectins, C-Type; D050794:STAT1 Transcription Factor; D020825:T-Box Domain Proteins; D014302:Trinitrobenzenesulfonic Acid; D000098815:T-bet Transcription Factor; D000099192:CD69 Antigens; C477508:jaceosidin