E. Bergseng

发表

Tetramer-visualized gluten-specific CD4+ T cells in blood as a potential diagnostic marker for coeliac disease without oral gluten challenge

A. Christophersen, M. Ráki, E. Bergseng, 2014, United European gastroenterology journal.

Unraveling the structural basis for the unusually rich association of human leukocyte antigen DQ2.5 with class-II-associated invariant chain peptides

M. Madhusudhan, E. Bergseng, L. Sollid, 2017, The Journal of Biological Chemistry.

Different binding motifs of the celiac disease-associated HLA molecules DQ2.5, DQ2.2, and DQ7.5 revealed by relative quantitative proteomics of endogenous peptide repertoires

Morten Nielsen, Ståle Nygård, Søren Buus, 2014, Immunogenetics.

Main Chain Hydrogen Bond Interactions in the Binding of Proline-rich Gluten Peptides to the Celiac Disease-associated HLA-DQ2 Molecule*

E. Bergseng, L. Sollid, Chu‐Young Kim, 2005, Journal of Biological Chemistry.

Differences in the risk of celiac disease associated with HLA-DQ2.5 or HLA-DQ2.2 are related to sustained gluten antigen presentation

E. Bergseng, L. Sollid, K. Hotta, 2009, Nature Immunology.

Analysis of the binding of gluten T-cell epitopes to various human leukocyte antigen class II molecules.

J. Sidney, A. Sette, E. Bergseng, 2008, Human immunology.

Antigen Presentation to Celiac Lesion-Derived T Cells of a 33-Mer Gliadin Peptide Naturally Formed by Gastrointestinal Digestion1

E. Bergseng, L. Sollid, S. Qiao, 2004, The Journal of Immunology.

Peptide Naturally Formed by Gastrointestinal Lesion-Derived T Cells of a 33-Mer Gliadin Antigen Presentation to Celiac

E. Bergseng, S. Qiao, Ø. Molberg, 2004 .

Assessing Possible Celiac Disease by an HLA-DQ2-gliadin Tetramer Test

M. Ráki, E. Bergseng, K. Lundin, 2011, The American Journal of Gastroenterology.

Direct cloning and tetramer staining to measure the frequency of intestinal gluten‐reactive T cells in celiac disease

M. Ráki, E. Bergseng, K. Lundin, 2013, European journal of immunology.

Soluble HLA-DQ2 expressed in S2 cells copurifies with a high affinity insect cell derived protein

E. Bergseng, L. Sollid, B. Fleckenstein, 2009, Immunogenetics.

Refining the Rules of Gliadin T Cell Epitope Binding to the Disease-Associated DQ2 Molecule in Celiac Disease: Importance of Proline Spacing and Glutamine Deamidation1

E. Bergseng, L. Sollid, S. Qiao, 2005, The Journal of Immunology.

Noninflammatory gluten peptide analogs as biomarkers for celiac sprue.

E. Bergseng, L. Sollid, C. Khosla, 2009, Chemistry & biology.

Inhibition of HLA-DQ2-mediated antigen presentation by analogues of a high affinity 33-residue peptide from alpha2-gliadin.

E. Bergseng, L. Sollid, Ludvig M Sollid, 2006, Journal of the American Chemical Society.

Structural basis for HLA-DQ2-mediated presentation of gluten epitopes in celiac disease

E. Bergseng, L. Sollid, Chu‐Young Kim, 2004, Proceedings of the National Academy of Sciences of the United States of America.

Plasma Cells Are the Most Abundant Gluten Peptide MHC-expressing Cells in Inflamed Intestinal Tissues From Patients With Celiac Disease.

Jeffrey J. Gray, Inger Sandlie, Jeliazko R. Jeliazkov, 2019, Gastroenterology.

Tetramer visualization of gut-homing gluten-specific T cells in the peripheral blood of celiac disease patients

M. Ráki, E. Bergseng, K. Lundin, 2007, Proceedings of the National Academy of Sciences.

Peptide binding to HLA-DQ2 and development of blocking agents for the treatment of celiac disease

E. Bergseng, 2008 .

Gluten-specific antibodies of celiac disease gut plasma cells recognize long proteolytic fragments that typically harbor T-cell epitopes

E. Bergseng, L. Sollid, M. Arntzen, 2016, Scientific Reports.

Healthy HLA-DQ2.5+ Subjects Lack Regulatory and Memory T Cells Specific for Immunodominant Gluten Epitopes of Celiac Disease

A. Christophersen, E. Bergseng, K. Lundin, 2016, The Journal of Immunology.

HLA-DQ2-restricted gluten-reactive T cells produce IL-21 but not IL-17 or IL-22

M. Ráki, E. Bergseng, K. Lundin, 2010, Mucosal Immunology.

Cyclic and dimeric gluten peptide analogues inhibiting DQ2-mediated antigen presentation in celiac disease.

Chu-Young Kim, E. Bergseng, L. Sollid, 2007, Bioorganic & medicinal chemistry.

Complexes of two cohorts of CLIP peptides and HLA-DQ2 of the autoimmune DR3-DQ2 haplotype are poor substrates for HLA-DM

E. Bergseng, L. Sollid, B. Fleckenstein, 2009, The Journal of Immunology.

Complexes of Two Cohorts of CLIP Peptides and HLA-DQ2 of the Autoimmune DR3-DQ2 Haplotype Are Poor Substrates for HLA-DM1

E. Bergseng, L. Sollid, B. Fleckenstein, 2008, The Journal of Immunology.

Haplotype Are Poor Substrates for HLA-DM and HLA-DQ2 of the Autoimmune DR3-DQ2 Complexes of Two Cohorts of CLIP Peptides

E. Bergseng, L. Sollid, B. Fleckenstein, 2008 .

Proline Spacing and Glutamine Deamidation Molecule in Celiac Disease : Importance of Binding to the Disease-Associated DQ 2 Refining the Rules of Gliadin T Cell Epitope

E. Bergseng, L. Sollid, S. Qiao, 2005 .

Small Bowel, Celiac Disease and Adaptive Immunity

A. Christophersen, E. Bergseng, K. Lundin, 2015, Digestive Diseases.

HLA-DQ Molecules as Affinity Matrix for Identification of Gluten T Cell Epitopes

A. Christophersen, E. Bergseng, L. Sollid, 2014, The Journal of Immunology.

A TCRα framework-centered codon shapes a biased T cell repertoire through direct MHC and CDR3β interactions.

E. Bergseng, K. Lundin, L. Sollid, 2017, JCI insight.

Evidence that HLA-DQ9 confers risk to celiac disease by presence of DQ9-restricted gluten-specific T cells.

E. Bergseng, K. Lundin, L. Sollid, 2012, Human immunology.

Erratum: Complexes of two cohorts of CLIP peptides and HLA-DQ2 of the autoimmune DR3-DQ2 haplotype are poor substrates for HLA-DM (The Journal of Immunology (2008) 181 (5451-5461))

Taejin Yoon, Ludvig M. Sollid, E. Bergseng, 2009 .