Advertisement

Two novel HLA-DQ2.5-restricted gluten T cell epitopes in the DQ2.5-glia-γ4 epitope family

  • Shuo-Wang QiaoEmail author
  • Ludvig M. Sollid
Short Communication

Abstract

Celiac disease is a chronic inflammatory condition of the small intestine caused by aberrant adaptive immune response to gluten protein from wheat and related cereal plants. Over 90% of celiac disease patients carry the HLA-DQ2.5 allotype and HLA-DQ2.5 presents gluten peptides to gluten-reactive CD4+ T cells in celiac disease patients. A large number of HLA-DQ2.5-restricted gluten T cell epitopes have been identified over the years. These epitopes are in general proline-rich and contain at least one glutamic acid residue that is generated from glutamine in the native gluten protein by deamidation. The deamidation is mediated by the enzyme transglutaminase 2 (TG2). It has been shown that the same T cell could recognize several different HLA-DQ2.5-restricted gluten T cell epitopes due to sequence similarities. In this paper, we demonstrate that three T cell clones derived from duodenal biopsies of different celiac disease patients are able to respond to at least five different gluten T cell epitopes within the DQ2.5-glia-γ4 epitope family, including two novel epitopes.

Keywords

Celiac disease T cell epitope Gluten T cell clone 

Notes

References

  1. Molberg Ø, McAdam SN, Lundin KEA, Sollid LM (2000) Studies of gliadin-specific T cells in celiac disease. In: Celiac disease - methods and protocols. Humana Press, Totowa, pp 105–124CrossRefGoogle Scholar
  2. Qiao SW, Bergseng E, Molberg O, Jung G, Fleckenstein B, Sollid LM (2005) Refining the rules of gliadin T cell epitope binding to the disease-associated DQ2 molecule in celiac disease: importance of proline spacing and glutamine deamidation. J Immunol 175:254–261CrossRefGoogle Scholar
  3. Sollid L, Qiao SW, Anderson R, Gianfrani C, Koning F (2012) Nomenclature and listing of celiac disease relevant gluten T-cell epitopes restricted by HLA-DQ molecules. Immunogenetics 64:455–460CrossRefGoogle Scholar

Copyright information

© Springer-Verlag GmbH Germany, part of Springer Nature 2019

Authors and Affiliations

  1. 1.KG Jebsen Coeliac Disease Research CentreUniversity of OsloOsloNorway
  2. 2.Department of ImmunologyOslo University HospitalOsloNorway

Personalised recommendations