Shuo Wang Qiao
Affiliation: University of Oslo
- Tissue transglutaminase-mediated formation and cleavage of histamine-gliadin complexes: biological effects and implications for celiac diseaseShuo Wang Qiao
Institute of Immunology, Rikshospitalet, University of Oslo, Oslo, Norway
J Immunol 174:1657-63. 2005..Interestingly, TG2 is able to hydrolyze the peptide-histamine conjugates when the concentrations of substrates are lowered, thereby releasing deamidated gluten peptides that are stimulatory to T cells...
- Refining the rules of gliadin T cell epitope binding to the disease-associated DQ2 molecule in celiac disease: importance of proline spacing and glutamine deamidationShuo Wang Qiao
Institute of Immunology, University of Oslo, Rikshospitalet University Hospital, Oslo, Norway
J Immunol 175:254-61. 2005..Contrary to previous findings, our data do not show selective presentation of DQ2.5 over DQ2.2 for gluten epitopes that carry proline residues at the P3 position...
- Antigen presentation to celiac lesion-derived T cells of a 33-mer gliadin peptide naturally formed by gastrointestinal digestionShuo Wang Qiao
Institute of Immunology, Rikshospitalet University Hospital, University of Oslo, Oslo, Norway
J Immunol 173:1757-62. 2004..The 33-mer is thus a potent T cell stimulator that does not require further processing within APC for T cell presentation and that binds to DQ2 with a pH profile that promotes extracellular binding...
- Gliadin T cell epitope selection by tissue transglutaminase in celiac disease. Role of enzyme specificity and pH influence on the transamidation versus deamidation processBurkhard Fleckenstein
Institute of Immunology, Rikshospitalet, University of Oslo, N 0027 Oslo, Norway
J Biol Chem 277:34109-16. 2002..This suggests that the deamidation of gluten peptides by TG2 more likely takes place in slightly acidic environments...
- The preferred substrates for transglutaminase 2 in a complex wheat gluten digest are Peptide fragments harboring celiac disease T-cell epitopesSiri Dørum
Centre for Immune Regulation, Institute of Immunology, University of Oslo, Oslo, Norway
PLoS ONE 5:e14056. 2010..In this study we aimed to identify the preferred peptide substrates of TG2 in a heterogeneous proteolytic digest of whole wheat gluten...
- Antigen presentation in celiac diseaseShuo Wang Qiao
Centre for Immune Regulation, Institute of Immunology, Rikshospitalet University Hospital and University of Oslo, Norway
Curr Opin Immunol 21:111-7. 2009..In comparison, DQ8 exhibits different binding characteristics, which may explain the lesser risk for disease in association with this molecule...
- Molecular characterization of covalent complexes between tissue transglutaminase and gliadin peptidesBurkhard Fleckenstein
Institute of Immunology, Rikshospitalet University Hospital, N 0027 Oslo, Norway
J Biol Chem 279:17607-16. 2004..The results are relevant to the understanding of how antibodies to TG2 are formed in celiac disease...
- A quantitative analysis of transglutaminase 2-mediated deamidation of gluten peptides: implications for the T-cell response in celiac diseaseSiri Dørum
Centre for Immune Regulation, Institute of Immunology, University of Oslo, and Rikshospitalet University Hospital, N 0027 Oslo, Norway
J Proteome Res 8:1748-55. 2009..Thus, the rate of deamidation by TG2 appears to be a factor of importance for the T-cell response to gluten in celiac disease...
- The adaptive immune response in celiac diseaseShuo Wang Qiao
Department of Immunology and Centre for Immune Regulation, University of Oslo, Oslo University Hospital Rikshospitalet, 0027, Oslo, Norway
Semin Immunopathol 34:523-40. 2012..Here we review recent developments in the understanding of the role of T cells, B cells, and antigen-presenting cells in the pathogenic immune response of this instructive disorder...
- High abundance of plasma cells secreting transglutaminase 2-specific IgA autoantibodies with limited somatic hypermutation in celiac disease intestinal lesionsRoberto Di Niro
Centre for Immune Regulation and Department of Immunology, University of Oslo and Oslo University Hospital Rikshospitalet, Oslo, Norway
Nat Med 18:441-5. 2012..This could result in preferential recruitment of plasma cells from naive IgD- and IgM-expressing B cells, thus possibly explaining why the antibody response to TG2 bears signs of a primary immune response despite the disease chronicity...
- Posttranslational modification of gluten shapes TCR usage in celiac diseaseShuo Wang Qiao
Department of Immunology, Centre for Immune Regulation, University of Oslo, 0027 Oslo, Norway
J Immunol 187:3064-71. 2011..The findings have implications for understanding T cell responses to posttranslationally modified Ags...
- Nomenclature and listing of celiac disease relevant gluten T-cell epitopes restricted by HLA-DQ moleculesLudvig M Sollid
Centre for Immune Regulation and Department of Immunology, University of Oslo and Oslo University Hospital, Rikshospitalet, Oslo, Norway
Immunogenetics 64:455-60. 2012..In this work, we give an overview of these epitopes and suggest a comprehensive, new nomenclature...
- Carcinoembryonic antigen-related cell adhesion molecule 1 inhibits proximal TCR signaling by targeting ZAP-70Zhangguo Chen
Gastroenterology Division, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA
J Immunol 180:6085-93. 2008..These studies show that long CT isoforms of CEACAM1 orchestrate an inhibitory program that abrogates extremely proximal events downstream of the TCR/CD3 complex by focusing on the activation of ZAP-70...
- Identification and analysis of multivalent proteolytically resistant peptides from gluten: implications for celiac sprueLu Shan
Department of Chemical Engineering, Stanford University, Stanford, CA 94305 5025, USA
J Proteome Res 4:1732-41. 2005....
- Dependence of antibody-mediated presentation of antigen on FcRnShuo Wang Qiao
Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 105:9337-42. 2008....
- SHP1 phosphatase-dependent T cell inhibition by CEACAM1 adhesion molecule isoformsTakashi Nagaishi
Gastroenterology Division, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
Immunity 25:769-81. 2006..Thus, CEACAM1 overexpression or deletion in T cells resulted in T cell inhibition or activation, respectively, revealing a role for CEACAM1 as a class of inhibitory receptors potentially amenable to therapeutic manipulation...