Allergy and Tissue Modelling Research Group, School of Molecular Medical Sciences, Queen's Medical Centre, The University of Nottingham, A Floor, West Block, Nottingham, NG7 2UH, UK.
BMC Immunol. 2012 Apr 16;13:20. doi: 10.1186/1471-2172-13-20.
Dendritic cells (DCs) are part of the innate immune system with a key role in initiating and modulating T cell mediated immune responses. Coeliac disease is caused by inappropriate activation of such a response leading to small intestinal inflammation when gluten is ingested. Tissue transglutaminase, an extracellular matrix (ECM) protein, has an established role in coeliac disease; however, little work to date has examined its impact on DCs. The aim of this study was to investigate the effect of small intestinal ECM proteins, fibronectin (FN) and tissue transglutaminase 2 (TG-2), on human DCs by including these proteins in DC cultures.The study used flow cytometry and scanning electron microscopy to determine the effect of FN and TG-2 on phenotype, endocytic ability and and morphology of DCs. Furthermore, DCs treated with FN and TG-2 were cultured with T cells and subsequent T cell proliferation and cytokine profile was determined.The data indicate that transglutaminase affected DCs in a concentration-dependent manner. High concentrations were associated with a more mature phenotype and increased ability to stimulate T cells, while lower concentrations led to maintenance of an immature phenotype.These data provide support for an additional role for transglutaminase in coeliac disease and demonstrate the potential of in vitro modelling of coeliac disease pathogenesis.
树突状细胞(DCs)是先天免疫系统的一部分,在启动和调节 T 细胞介导的免疫反应中起着关键作用。乳糜泻是由这种反应的不当激活引起的,当摄入麸质时会导致小肠炎症。组织转谷氨酰胺酶是一种细胞外基质(ECM)蛋白,在乳糜泻中具有既定的作用;然而,迄今为止,很少有研究检查其对 DCs 的影响。本研究旨在通过在 DC 培养物中包含这些蛋白质,研究小肠 ECM 蛋白纤维连接蛋白(FN)和组织转谷氨酰胺酶 2(TG-2)对人 DCs 的影响。该研究使用流式细胞术和扫描电子显微镜来确定 FN 和 TG-2 对 DC 表型、内吞能力和形态的影响。此外,用 FN 和 TG-2 处理的 DC 与 T 细胞共培养,并确定随后的 T 细胞增殖和细胞因子谱。数据表明转谷氨酰胺酶以浓度依赖的方式影响 DCs。高浓度与更成熟的表型和增强刺激 T 细胞的能力相关,而较低浓度则导致维持不成熟的表型。这些数据为转谷氨酰胺酶在乳糜泻中的额外作用提供了支持,并证明了乳糜泻发病机制的体外模拟的潜力。