Tissue transglutaminase treatment leads to concentration-dependent changes in dendritic cell phenotype - implications for the role of transglutaminase in coeliac disease

BMC Immunology

Research Article

William J Dalleywater¹  Amir M Ghaemmaghami¹  David YS Chau¹ 

[1] Allergy and Tissue Modelling Research Group, School of Molecular Medical Sciences, Queen's Medical Centre, The University of Nottingham, NG7 2UH, A Floor, West Block, Nottingham, UK;

关键词: Coeliac disease;    Dendritic cells;    Immune response;    Gliadin;    Tissue engineering;    Transglutaminase;   

DOI  :  10.1186/1471-2172-13-20

 received in 2011-12-15, accepted in 2012-04-16,  发布年份 2012

来源: Springer

【 摘 要 】

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.

【 授权许可】

Unknown   
© Dalleywater et al; licensee BioMed Central Ltd. 2012. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.