title: Increased expression of mGITRL on D2SC/1 cells by particulate β-glucan impairs the suppressive effect of CD4+CD25+ regulatory T cells and enhances the effector T cell proliferation.
abstract: β-Glucans have been shown to enhance immune responses for centuries, which contributes to their anti-tumor property. However, their mechanisms of action are still elusive. Dectin-1, the C-type lectin receptor for β-glucan, is expressed abundantly on dendritic cells (DCs). Activation of DCs via Dectin-1 can lead to the maturation of DC, inducing both innate and adaptive immune responses against tumor development and microbial infection. In this study, we found that particulate yeast-derived β-glucans could induce the maturation of murine dendritic cell line D2SC/1 cells and increase the expression of mGITRL on D2SC/1 cells via Dectin-1/Syk pathway in a dose dependent manner. Furthermore, we demonstrated that the increased mGITRL on D2SC/1 cells could impair the suppressive activity of CD4(+)CD25(+) regulatory T cells (Tregs) and enhance the proliferation of CD4(+)CD25(-) effector T cells (Teffs). These findings suggest that particulate β-glucan can be used as immunomodulator to stimulate potent T cell-mediated adaptive immunity while down-regulate immune suppressive activity, leading to a more efficient defense mechanism against tumor development or infectious diseases.
authors.affiliation: The Affiliated People's Hospital, and School of Medical Science and Laboratory Medicine, Jiangsu University, Zhenjiang, Jiangsu Province, PR China.
authors.forename: Jie
authors.initials: J
authors.lastname: Tian
authors.forename: Jie
authors.initials: J
authors.lastname: Ma
authors.forename: Shengjun
authors.initials: S
authors.lastname: Wang
authors.forename: Jun
authors.initials: J
authors.lastname: Yan
authors.forename: Jianguo
authors.initials: J
authors.lastname: Chen
authors.forename: Jia
authors.initials: J
authors.lastname: Tong
authors.forename: Chaoyang
authors.initials: C
authors.lastname: Wu
authors.forename: Yingzhao
authors.initials: Y
authors.lastname: Liu
authors.forename: Bin
authors.initials: B
authors.lastname: Ma
authors.forename: Chaoming
authors.initials: C
authors.lastname: Mao
authors.forename: Zhijun
authors.initials: Z
authors.lastname: Jiao
authors.forename: Qixiang
authors.initials: Q
authors.lastname: Shao
authors.forename: Liwei
authors.initials: L
authors.lastname: Lu
authors.forename: Huaxi
authors.initials: H
authors.lastname: Xu
mesh_terms: D056704:Adaptive Immunity / Q000187:drug effects; D000818:Animals; D001483:Base Sequence; D002460:Cell Line; D049109:Cell Proliferation / Q000187:drug effects; D003713:Dendritic Cells / Q000187:drug effects / Q000276:immunology*; D004306:Dose-Response Relationship, Immunologic; D015870:Gene Expression / Q000187:drug effects; D007155:Immunologic Factors / Q000008:administration & dosage / Q000494:pharmacology; D066298:In Vitro Techniques; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D012333:RNA, Messenger / Q000235:genetics; D016176:T-Lymphocyte Subsets / Q000166:cytology / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*; D048069:Tumor Necrosis Factors / Q000235:genetics*; D047071:beta-Glucans / Q000008:administration & dosage / Q000276:immunology* / Q000494:pharmacology*
chemical_list: D007155:Immunologic Factors; D012333:RNA, Messenger; C478966:Tnfsf18 protein, mouse; D048069:Tumor Necrosis Factors; D047071:beta-Glucans