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首页> 外文期刊>International immunopharmacology >Bone marrow CD11b(+)F4/80(+) dendritic cells ameliorate collagen-induced arthritis through modulating the balance between Treg and Th17
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Bone marrow CD11b(+)F4/80(+) dendritic cells ameliorate collagen-induced arthritis through modulating the balance between Treg and Th17

机译：骨髓CD11b（+）F4 / 80（+）树突状细胞通过调节Treg和Th17之间的平衡来改善胶原蛋白诱发的关节炎

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Tolerogenic dendritic cells (DCs) are well-known to show an immunosuppressive function. In this study we determine the therapeutic effects and potential mechanisms of transferred bone marrow (BM) CD11b(+)F4/80(+) DCs on collagen-induced arthritis (CIA) in mice. Murine BM CD11b(+)F4/80(+) DCs were generated under the stimulation of GM-CSF and IL-4, and the function of BM CD11b(+)F4/80(+) DCs was identified by measuring the levels of IL10, TGF-beta and indoleamine 23-dioxygenase (IDO). BM CD11b(+)F4/80(+) DCs were transferred to CIA mice by intravenous injections. The histopathology of joint and spleen were evaluated. T lymphocyte proliferation, Treg and Th17 subsets were analyzed. The expressions of Foxp3, Helios and ROR gamma t in T lymphocytes co-cultured with BM CD11b(+)F4/80(+) DCs were measured in vitro. We found that BM CD11b(+)F4/80(+) DCs induced by GMCSF and IL-4 could express high levels of IL-10 TGF-beta and IDO. BM CD11b(+)F4/80(+) DCs significantly reduced the pathologic scores in joints and spleens, which correlated significantly with the reduced T lymphocyte proliferation and Th17 cell number, and with the increased Tregs number. In vitro, OVA-pulsed BM CD11b(+)F4/80(+) DCs promoted Treg cell expansion, enhanced IL-10 and CTLA-4 protein expression, augmented Foxp3 and Helios mRNA expression, and inhibited ROR gamma t and IL-17 mRNA expression. Taken together, BM CD11b(+)F4/80(+) DCs are able to ameliorate the development and severity of CIA, at least partly by inducing Foxp3 Treg cell expansion and suppressing Th17 function. The BM CD11b(+)F4/80(+) DCs might have a promising immunotherapeutic potential for autoimmune arthritis. (C) 2015 Elsevier B.V. All rights reserved.
机译：众所周知，致耐受性树突状细胞（DC）具有免疫抑制功能。在这项研究中，我们确定了转移性骨髓（BM）CD11b（+）F4 / 80（+）DC对小鼠胶原诱导的关节炎（CIA）的治疗作用和潜在机制。在GM-CSF和IL-4的刺激下产生了小鼠BM CD11b（+）F4 / 80（+）DCs，并通过测量BMCD11b（+）F4 / 80（+）DC的水平来鉴定其功能。 IL10，TGF-β和吲哚胺23-双加氧酶（IDO）。通过静脉注射将BM CD11b（+）F4 / 80（+）DC转移到CIA小鼠中。评价关节和脾的组织病理学。分析T淋巴细胞增殖，Treg和Th17亚群。在体外测量与BM CD11b（+）F4 / 80（+）DC共培养的T淋巴细胞中Foxp3，Helios和RORγt的表达。我们发现，GMCSF和IL-4诱导的BM CD11b（+）F4 / 80（+）DC可以表达高水平的IL-10 TGF-beta和IDO。 BM CD11b（+）F4 / 80（+）DC显着降低了关节和脾脏的病理评分，这与T淋巴细胞增殖减少和Th17细胞数减少以及Tregs数目增加显着相关。在体外，OVA刺激的BM CD11b（+）F4 / 80（+）DC促进Treg细胞扩增，增强IL-10和CTLA-4蛋白表达，增强Foxp3和Helios mRNA表达，并抑制RORγt和IL-17 mRNA表达。综上所述，BM CD11b（+）F4 / 80（+）DC能够至少部分地通过诱导Foxp3 Treg细胞扩增并抑制Th17功能来改善CIA的发展和严重程度。 BM CD11b（+）F4 / 80（+）DC可能具有针对自身免疫性关节炎的有希望的免疫治疗潜力。 （C）2015 Elsevier B.V.保留所有权利。

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