Antigens, CD19

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  Subject Areas on Research

  • A CD19-dependent signaling pathway regulates autoimmunity in Lyn-deficient mice. 
  • A c-Myc and surface CD19 signaling amplification loop promotes B cell lymphoma development and progression in mice. 
  • A glycoengineered anti-CD19 antibody with potent antibody-dependent cellular cytotoxicity activity in vitro and lymphoma growth inhibition in vivo. 
  • A novel subset of memory B cells is enriched in autoreactivity and correlates with adverse outcomes in SLE. 
  • A role for CD21/CD35 and CD19 in responses to acute septic peritonitis: a potential mechanism for mast cell activation. 
  • A sensitized genetic system for the analysis of murine B lymphocyte signal transduction pathways dependent on Bruton's tyrosine kinase. 
  • Abnormal B lymphocyte development, activation, and differentiation in mice that lack or overexpress the CD19 signal transduction molecule. 
  • Altered B lymphocyte function induces systemic autoimmunity in systemic sclerosis. 
  • Association of a functional CD19 polymorphism with susceptibility to systemic sclerosis. 
  • B Lymphocyte signaling established by the CD19/CD22 loop regulates autoimmunity in the tight-skin mouse. 
  • B lymphocytes contribute to autoimmune disease pathogenesis: current trends and clinical implications. 
  • B lymphocytes differentially influence acute and chronic allograft rejection in mice. 
  • B-1a and B-1b cells exhibit distinct developmental requirements and have unique functional roles in innate and adaptive immunity to S. pneumoniae. 
  • B-cell depletion in vitro and in vivo with an afucosylated anti-CD19 antibody. 
  • Biochemical and immunological abnormalities in purine nucleoside phosphorylase deficient mice. 
  • CD19 amplification of B lymphocyte Ca2+ responses: a role for Lyn sequestration in extinguishing negative regulation. 
  • CD19 amplifies B lymphocyte signal transduction by regulating Src-family protein tyrosine kinase activation. 
  • CD19 and CD22 expression reciprocally regulates tyrosine phosphorylation of Vav protein during B lymphocyte signaling. 
  • CD19 and CD22 regulate a B lymphocyte signal transduction pathway that contributes to autoimmunity. 
  • CD19 can regulate B lymphocyte signal transduction independent of complement activation. 
  • CD19 expression in B cells is important for suppression of contact hypersensitivity. 
  • CD19 expression in B cells regulates atopic dermatitis in a mouse model. 
  • CD19 expression levels regulate B lymphocyte development: human CD19 restores normal function in mice lacking endogenous CD19. 
  • CD19 hyperexpression augments Sle1-induced humoral autoimmunity but not clinical nephritis. 
  • CD19 maps to a region of conservation between human chromosome 16 and mouse chromosome 7. 
  • CD19 regulates B lymphocyte responses to transmembrane signals. 
  • CD19 regulates B lymphocyte signaling thresholds critical for the development of B-1 lineage cells and autoimmunity. 
  • CD19 regulates Src family protein tyrosine kinase activation in B lymphocytes through processive amplification. 
  • CD19 regulates innate immunity by the toll-like receptor RP105 signaling in B lymphocytes. 
  • CD19 regulates intrinsic B lymphocyte signal transduction and activation through a novel mechanism of processive amplification. 
  • CD19 regulates skin and lung fibrosis via Toll-like receptor signaling in a model of bleomycin-induced scleroderma. 
  • CD19 regulates the development of bleomycin-induced pulmonary fibrosis in a mouse model. 
  • CD19, CD21, and CD22: multifaceted response regulators of B lymphocyte signal transduction. 
  • CD19, a response regulator of B lymphocytes, regulates wound healing through hyaluronan-induced TLR4 signaling. 
  • CD19-CD21 complex regulates an intrinsic Src family kinase amplification loop that links innate immunity with B-lymphocyte intracellular calcium responses. 
  • CD19-dependent B lymphocyte signaling thresholds influence skin fibrosis and autoimmunity in the tight-skin mouse. 
  • CD19-regulated signaling thresholds control peripheral tolerance and autoantibody production in B lymphocytes. 
  • CD19: a promising B cell target for rheumatoid arthritis. 
  • CD21/35 promotes protective immunity to Streptococcus pneumoniae through a complement-independent but CD19-dependent pathway that regulates PD-1 expression. 
  • Characterization of an Epstein-Barr virus receptor on human epithelial cells. 
  • Collagen type-V is a danger signal associated with primary graft dysfunction in lung transplantation. 
  • Complement component C3d-antigen complexes can either augment or inhibit B lymphocyte activation and humoral immunity in mice depending on the degree of CD21/CD19 complex engagement. 
  • Complementary roles for CD19 and Bruton's tyrosine kinase in B lymphocyte signal transduction. 
  • Differential phosphorylation of functional tyrosines in CD19 modulates B-lymphocyte activation. 
  • Donor-derived regulatory B cells are important for suppression of murine sclerodermatous chronic graft-versus-host disease. 
  • Hapten-induced primary and memory humoral responses are inhibited by the infusion of anti-CD20 monoclonal antibody (IDEC-C2B8, Rituximab). 
  • High frequency of immunophenotype changes in acute myeloid leukemia at relapse: implications for residual disease detection (Cancer and Leukemia Group B Study 8361). 
  • Humoral autoimmunity in mice overexpressing B cell surface CD19: vital role for MHC class II. 
  • IL-10-producing regulatory B10 cells inhibit intestinal injury in a mouse model. 
  • Immune signatures in follicular lymphoma. 
  • Immunological findings in thymoma and thymoma-related syndromes. 
  • Immunotherapy using unconjugated CD19 monoclonal antibodies in animal models for B lymphocyte malignancies and autoimmune disease. 
  • Inhibitory role of CD19 in the progression of experimental autoimmune encephalomyelitis by regulating cytokine response. 
  • Innate and adaptive receptors interact to balance humoral immunity. 
  • Intersection of the complement and immune systems: a signal transduction complex of the B lymphocyte-containing complement receptor type 2 and CD19. 
  • Intravital imaging of Ca(2+) signals in lymphocytes of Ca(2+) biosensor transgenic mice: indication of autoimmune diseases before the pathological onset. 
  • Isolation of cDNAs encoding the CD19 antigen of human and mouse B lymphocytes. A new member of the immunoglobulin superfamily. 
  • Loss of tolerance of anti-dsDNA B cells in mice overexpressing CD19. 
  • Lupus-specific antiribonucleoprotein B cell tolerance in nonautoimmune mice is maintained by differentiation to B-1 and governed by B cell receptor signaling thresholds. 
  • Modulation of B lymphocyte antigen receptor signal transduction by a CD19/CD22 regulatory loop. 
  • Ordinary Differential Equation Models for Adoptive Immunotherapy. 
  • Prolonged B-cell depletion in MuSK myasthenia gravis following rituximab treatment. 
  • Quantitative determination of surface antibody binding capacities of immune subsets present in peripheral blood of healthy adult donors. 
  • Quantitative genetic variation in CD19 expression correlates with autoimmunity. 
  • Regulation of B lymphocyte development and activation by the CD19/CD21/CD81/Leu 13 complex requires the cytoplasmic domain of CD19. 
  • Regulation of B-cell development by BCAP and CD19 through their binding to phosphoinositide 3-kinase. 
  • Regulatory B cell (B10 Cell) expansion during Listeria infection governs innate and cellular immune responses in mice. 
  • Regulatory B cells (B10 cells) and regulatory T cells have independent roles in controlling experimental autoimmune encephalomyelitis initiation and late-phase immunopathogenesis. 
  • Regulatory B cells (B10 cells) have a suppressive role in murine lupus: CD19 and B10 cell deficiency exacerbates systemic autoimmunity. 
  • Regulatory B cells control T-cell autoimmunity through IL-21-dependent cognate interactions. 
  • Regulatory B cells suppress imiquimod-induced, psoriasis-like skin inflammation. 
  • Risk of HBV reactivation post CD19-CAR-T cell therapy in DLBCL patients with concomitant chronic HBV infection. 
  • Role of the CD19 and CD21/35 receptor complex in innate immunity, host defense and autoimmunity. 
  • Similar CD19 dysregulation in two autoantibody-associated autoimmune diseases suggests a shared mechanism of B-cell tolerance loss. 
  • Structure and domain organization of the CD19 antigen of human, mouse, and guinea pig B lymphocytes. Conservation of the extensive cytoplasmic domain. 
  • Structure of the genes encoding the CD19 antigen of human and mouse B lymphocytes. 
  • T cells or active Epstein-Barr virus infection in the development of lymphoproliferative disease in human B cell-injected severe combined immunodeficient mice. 
  • The CD19 signal transduction complex of B lymphocytes. Deletion of the CD19 cytoplasmic domain alters signal transduction but not complex formation with TAPA-1 and Leu 13. 
  • The CD19 signal transduction molecule is a response regulator of B-lymphocyte differentiation. 
  • The CD19-CD21 complex regulates signal transduction thresholds governing humoral immunity and autoimmunity. 
  • The CD19-CD21 signal transduction complex of B lymphocytes regulates the balance between health and autoimmune disease: systemic sclerosis as a model system. 
  • The CD19/CD21 signal transducing complex of human B lymphocytes includes the target of antiproliferative antibody-1 and Leu-13 molecules. 
  • The CD19/CD21 signal transduction complex of B lymphocytes. 
  • The Tumor Microenvironment Regulates CD19 and CD20 Immunotherapy for Lymphoma. 
  • The c-Abl tyrosine kinase is regulated downstream of the B cell antigen receptor and interacts with CD19. 
  • The human fetal lymphocyte lineage: identification by CD27 and LIN28B expression in B cell progenitors. 
  • The tetraspanin CD81 regulates the expression of CD19 during B cell development in a postendoplasmic reticulum compartment. 
  • Tisagenlecleucel in Children and Young Adults with B-Cell Lymphoblastic Leukemia. 
  • Tissue-specific expression of the human CD19 gene in transgenic mice inhibits antigen-independent B-lymphocyte development. 
  • Transmembrane signals generated through MHC class II, CD19, CD20, CD39, and CD40 antigens induce LFA-1-dependent and independent adhesion in human B cells through a tyrosine kinase-dependent pathway. 
  • Tumor-targeted T cells modified to secrete IL-12 eradicate systemic tumors without need for prior conditioning.