Abundance and unique repertoire of plasma cells secreting IgA autoantibodies to transglutaminase 2 in the intestinal lesion of celiac disease

[1]  K. Lundin,et al.  Long-Lived Plasma Cells from Human Small Intestine Biopsies Secrete Immunoglobulins for Many Weeks In Vitro , 2011, The Journal of Immunology.

[2]  M. Ráki,et al.  Posttranslational Modification of Gluten Shapes TCR Usage in Celiac Disease , 2011, The Journal of Immunology.

[3]  J. Clarke,et al.  What is a systematic review? , 2011, Evidence Based Nursing.

[4]  H. Wardemann,et al.  The majority of intestinal IgA+ and IgG+ plasmablasts in the human gut are antigen-specific. , 2011, The Journal of clinical investigation.

[5]  Michael Meyer-Hermann,et al.  Germinal Center Dynamics Revealed by Multiphoton Microscopy with a Photoactivatable Fluorescent Reporter , 2010, Cell.

[6]  F. Lund-Johansen,et al.  Rapid Generation of Rotavirus-Specific Human Monoclonal Antibodies from Small-Intestinal Mucosa , 2010, The Journal of Immunology.

[7]  K. Kaukinen,et al.  Celiac disease without villous atrophy in children: a prospective study. , 2010, The Journal of pediatrics.

[8]  C. Goodnow,et al.  Control systems and decision making for antibody production , 2010, Nature Immunology.

[9]  M. Heikenwalder,et al.  Reversible Microbial Colonization of Germ-Free Mice Reveals the Dynamics of IgA Immune Responses , 2010, Science.

[10]  K. Lynch,et al.  Screening Detects a High Proportion of Celiac Disease in Young HLA-genotyped Children , 2010, Journal of pediatric gastroenterology and nutrition.

[11]  F. Paparo,et al.  High density of intraepithelial γδ lymphocytes and deposits of immunoglobulin (Ig)M anti‐tissue transglutaminase antibodies in the jejunum of coeliac patients with IgA deficiency , 2009, Clinical and experimental immunology.

[12]  Uri Hershberg,et al.  Taking Advantage: High-Affinity B Cells in the Germinal Center Have Lower Death Rates, but Similar Rates of Division, Compared to Low-Affinity Cells1 , 2009, The Journal of Immunology.

[13]  R. Brink,et al.  Antigen Affinity Controls Rapid T-Dependent Antibody Production by Driving the Expansion Rather than the Differentiation or Extrafollicular Migration of Early Plasmablasts1 , 2009, The Journal of Immunology.

[14]  Richard T. Wyatt,et al.  Broad diversity of neutralizing antibodies isolated from memory B cells in HIV-infected individuals , 2009, Nature.

[15]  Andreas Radbruch,et al.  Blood-borne human plasma cells in steady state are derived from mucosal immune responses. , 2009, Blood.

[16]  J. Wrammert,et al.  Rapid generation of fully human monoclonal antibodies specific to a vaccinating antigen , 2009, Nature Protocols.

[17]  B. Nakken,et al.  Functional anergy in a subpopulation of naive B cells from healthy humans that express autoreactive immunoglobulin receptors , 2009, The Journal of experimental medicine.

[18]  Hedda Wardemann,et al.  B-cell tolerance checkpoints in health and autoimmunity. , 2008, Current opinion in immunology.

[19]  L. Sollid,et al.  The propensity for deamidation and transamidation of peptides by transglutaminase 2 is dependent on substrate affinity and reaction conditions. , 2008, Biochimica et biophysica acta.

[20]  Paolo Casali,et al.  Nature and functions of autoantibodies , 2008, Nature Clinical Practice Rheumatology.

[21]  Patrick C. Wilson,et al.  Rapid cloning of high-affinity human monoclonal antibodies against influenza virus , 2008, Nature.

[22]  A. Plebani,et al.  Intestinal bacteria trigger T cell-independent immunoglobulin A(2) class switching by inducing epithelial-cell secretion of the cytokine APRIL. , 2007, Immunity.

[23]  P. Wilson,et al.  Mature B cells class switched to IgD are autoreactive in healthy individuals. , 2007, The Journal of clinical investigation.

[24]  M. Nussenzweig,et al.  Autoreactivity in human IgG+ memory B cells. , 2007, Immunity.

[25]  Kenneth G. C. Smith,et al.  Competence and competition: the challenge of becoming a long-lived plasma cell , 2006, Nature Reviews Immunology.

[26]  L. Lorand,et al.  Endomysial antibody-negative coeliac disease: clinical characteristics and intestinal autoantibody deposits , 2006, Gut.

[27]  D. Schuppan,et al.  Cross linking to tissue transglutaminase and collagen favours gliadin toxicity in coeliac disease , 2005, Gut.

[28]  D. Moher,et al.  The diagnostic accuracy of serologic tests for celiac disease: a systematic review. , 2005, Gastroenterology.

[29]  P. Green.  The many faces of celiac disease: clinical presentation of celiac disease in the adult population. , 2005, Gastroenterology.

[30]  K. Toellner,et al.  Extrafollicular antibody responses , 2003, Immunological reviews.

[31]  L. Sollid.  Coeliac disease: dissecting a complex inflammatory disorder , 2002, Nature Reviews Immunology.

[32]  F. Paparo,et al.  Anti-tissue transglutaminase antibodies from coeliac patients inhibit transglutaminase activity both in vitro and in situ , 2002, Gut.

[33]  K. Toellner,et al.  Low-level Hypermutation in T Cell–independent Germinal Centers Compared with High Mutation Rates Associated with T Cell–dependent Germinal Centers , 2002, The Journal of experimental medicine.

[34]  R. Zinkernagel,et al.  A primitive T cell-independent mechanism of intestinal mucosal IgA responses to commensal bacteria. , 2000, Science.

[35]  L. Boursier,et al.  Characteristics of IgVH genes used by human intestinal plasma cells from childhood , 1999, Immunology.

[36]  I. Korponay-Szabó,et al.  Tissue transglutaminase autoantibody enzyme-linked immunosorbent assay in detecting celiac disease. , 1998, Gastroenterology.

[37]  F. Koning,et al.  Selective deamidation by tissue transglutaminase strongly enhances gliadin-specific T cell reactivity. , 1998, Journal of immunology.

[38]  M. Neuberger,et al.  Affinity dependence of the B cell response to antigen: a threshold, a ceiling, and the importance of off-rate. , 1998, Immunity.

[39]  L. Fugger,et al.  Tissue transglutaminase selectively modifies gliadin peptides that are recognized by gut-derived T cells in celiac disease , 1998, Nature Medicine.

[40]  K. Lundin,et al.  Autoantibodies in coeliac disease: tissue transglutaminase—guilt by association? , 1997, Gut.

[41]  D. Schuppan,et al.  Identification of tissue transglutaminase as the autoantigen of celiac disease , 1997, Nature Medicine.

[42]  K. Shokat,et al.  Antigen-induced B-cell death and elimination during germinal-centre immune responses , 1995, Nature.

[43]  T. Halstensen,et al.  Association of subepithelial deposition of activated complement and immunoglobulin G and M response to gluten in celiac disease. , 1992, Gastroenterology.

[44]  C. Alberini,et al.  Developmental regulation of IgM secretion: The role of the carboxy-terminal cysteine , 1990, Cell.

[45]  D. Parker.  Stimulation of mouse lymphocytes by insoluble anti-mouse immunoglobulin , 1975, Nature.

[46]  I. Mahé,et al.  The Vote of Acute Medical Inpatients , 2009, Journal of aging and health.

[47]  E. Butcher,et al.  A major peritoneal reservoir of precursors for intestinal IgA plasma cells. , 1989, Immunological investigations.