Shuo Wang Qiao

Summary

Affiliation: University of Oslo
Country: Norway

Publications

  1. ncbi request reprint Tissue transglutaminase-mediated formation and cleavage of histamine-gliadin complexes: biological effects and implications for celiac disease
    Shuo Wang Qiao
    Institute of Immunology, Rikshospitalet, University of Oslo, Oslo, Norway
    J Immunol 174:1657-63. 2005
  2. ncbi request reprint 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
    Shuo Wang Qiao
    Institute of Immunology, University of Oslo, Rikshospitalet University Hospital, Oslo, Norway
    J Immunol 175:254-61. 2005
  3. ncbi request reprint Antigen presentation to celiac lesion-derived T cells of a 33-mer gliadin peptide naturally formed by gastrointestinal digestion
    Shuo Wang Qiao
    Institute of Immunology, Rikshospitalet University Hospital, University of Oslo, Oslo, Norway
    J Immunol 173:1757-62. 2004
  4. ncbi request reprint Gliadin T cell epitope selection by tissue transglutaminase in celiac disease. Role of enzyme specificity and pH influence on the transamidation versus deamidation process
    Burkhard Fleckenstein
    Institute of Immunology, Rikshospitalet, University of Oslo, N 0027 Oslo, Norway
    J Biol Chem 277:34109-16. 2002
  5. pmc The preferred substrates for transglutaminase 2 in a complex wheat gluten digest are Peptide fragments harboring celiac disease T-cell epitopes
    Siri Dørum
    Centre for Immune Regulation, Institute of Immunology, University of Oslo, Oslo, Norway
    PLoS ONE 5:e14056. 2010
  6. doi request reprint Antigen presentation in celiac disease
    Shuo Wang Qiao
    Centre for Immune Regulation, Institute of Immunology, Rikshospitalet University Hospital and University of Oslo, Norway
    Curr Opin Immunol 21:111-7. 2009
  7. ncbi request reprint Molecular characterization of covalent complexes between tissue transglutaminase and gliadin peptides
    Burkhard Fleckenstein
    Institute of Immunology, Rikshospitalet University Hospital, N 0027 Oslo, Norway
    J Biol Chem 279:17607-16. 2004
  8. doi request reprint A quantitative analysis of transglutaminase 2-mediated deamidation of gluten peptides: implications for the T-cell response in celiac disease
    Siri 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
  9. doi request reprint The adaptive immune response in celiac disease
    Shuo 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
  10. doi request reprint High abundance of plasma cells secreting transglutaminase 2-specific IgA autoantibodies with limited somatic hypermutation in celiac disease intestinal lesions
    Roberto 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

Collaborators

Detail Information

Publications16

  1. ncbi request reprint Tissue transglutaminase-mediated formation and cleavage of histamine-gliadin complexes: biological effects and implications for celiac disease
    Shuo 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...
  2. ncbi request reprint 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
    Shuo 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...
  3. ncbi request reprint Antigen presentation to celiac lesion-derived T cells of a 33-mer gliadin peptide naturally formed by gastrointestinal digestion
    Shuo 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...
  4. ncbi request reprint Gliadin T cell epitope selection by tissue transglutaminase in celiac disease. Role of enzyme specificity and pH influence on the transamidation versus deamidation process
    Burkhard 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...
  5. pmc The preferred substrates for transglutaminase 2 in a complex wheat gluten digest are Peptide fragments harboring celiac disease T-cell epitopes
    Siri 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...
  6. doi request reprint Antigen presentation in celiac disease
    Shuo 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...
  7. ncbi request reprint Molecular characterization of covalent complexes between tissue transglutaminase and gliadin peptides
    Burkhard 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...
  8. doi request reprint A quantitative analysis of transglutaminase 2-mediated deamidation of gluten peptides: implications for the T-cell response in celiac disease
    Siri 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...
  9. doi request reprint The adaptive immune response in celiac disease
    Shuo 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...
  10. doi request reprint High abundance of plasma cells secreting transglutaminase 2-specific IgA autoantibodies with limited somatic hypermutation in celiac disease intestinal lesions
    Roberto 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...
  11. doi request reprint Posttranslational modification of gluten shapes TCR usage in celiac disease
    Shuo 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...
  12. pmc Nomenclature and listing of celiac disease relevant gluten T-cell epitopes restricted by HLA-DQ molecules
    Ludvig 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...
  13. ncbi request reprint Carcinoembryonic antigen-related cell adhesion molecule 1 inhibits proximal TCR signaling by targeting ZAP-70
    Zhangguo 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...
  14. pmc Identification and analysis of multivalent proteolytically resistant peptides from gluten: implications for celiac sprue
    Lu Shan
    Department of Chemical Engineering, Stanford University, Stanford, CA 94305 5025, USA
    J Proteome Res 4:1732-41. 2005
    ....
  15. pmc Dependence of antibody-mediated presentation of antigen on FcRn
    Shuo 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
    ....
  16. ncbi request reprint SHP1 phosphatase-dependent T cell inhibition by CEACAM1 adhesion molecule isoforms
    Takashi 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...