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Animal models of spondyloarthritis.

机译:脊椎关节炎的动物模型。

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PURPOSE OF REVIEW: The aim of this article is to review new insights into spondyloarthritis obtained in animal models during the last year. RECENT FINDINGS: HLA-B27 misfolding has been demonstrated in HLA-B27/human beta2-microglobulin transgenic rats. HLA-B27 misfolding is associated with a typical unfolded protein stress response and with an interferon-response signature. Prebiotic treatment of these rats reduced colitis and arthritis. Proteoglycan-induced spondylitis is distinct from proteoglycan-induced arthritis. Specific susceptibility loci for proteoglycan-induced spondylitis have been demonstrated. Bone morphogenetic proteins are important in new cartilage and bone formation in ankylosing enthesitis. Psoriasis and psoriatic arthritis-like disease develops in conditional double JunB/c-Jun knockout mice. SUMMARY: Insights into the molecular signaling pathways driving HLA-B27 associated spondylitis, autoimmune spondylitis, ankylosing enthesitis and psoriasis, resulting from animal models, identify new and specific therapeutic targets in spondyloarthritis.
机译:审查的目的:本文的目的是回顾对去年动物模型中获得的脊椎关节炎的新见解。最近的发现:在HLA-B27 /人beta2-微球蛋白转基因大鼠中已证明HLA-B27错折叠。 HLA-B27错折叠与典型的未折叠蛋白应激反应和干扰素反应特征相关。这些大鼠的益生元治疗减少了结肠炎和关节炎。蛋白聚糖诱导的脊柱炎与蛋白聚糖诱导的关节炎不同。已经证明了蛋白聚糖诱导的脊椎炎的特异性易感基因座。骨形态发生蛋白在强直性皮炎中的新软骨和骨骼形成中很重要。有条件的双重JunB / c-Jun基因敲除小鼠患上牛皮癣和牛皮癣性关节炎样疾病。摘要:动物模型导致的驱动HLA-B27相关性脊柱炎,自身免疫性脊柱炎,强直性皮炎和牛皮癣的分子信号通路的见解确定了脊椎关节炎的新的和特定的治疗靶标。

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