Qualitative regulation of B cell antigen receptor signaling by CD19: selective requirement for PI3-kinase activation, inositol-1,4,5-trisphosphate production and Ca2+ mobilization

J Exp Med. 1997 Dec 1;186(11):1897-910. doi: 10.1084/jem.186.11.1897.

Abstract

Genetic ablation of the B cell surface glycoprotein CD19 severely impairs the humoral immune response. This requirement is thought to reflect a critical role of CD19 in signal transduction that occurs upon antigen C3dg coligation of antigen receptors with CD19 containing type 2 complement receptors (CR2). Here we show that CD19 plays a key accessory role in B cell antigen receptor signaling independent of CR2 coligation and define molecular circuitry by which this function is mediated. While CD19 is not required for antigen-mediated activation of receptor proximal tyrosines kinases, it is critical for activation of phosphatidylinositol 3-kinase (PI3-kinase). PI3-Kinase activation is dependent on phosphorylation of CD19 Y484 and Y515. Antigen-induced CD19-dependent PI3-kinase activation is required for normal phosphoinositide hydrolysis and Ca2+ mobilization responses. Thus, CD19 functions as a B cell antigen receptor accessory molecule that modifies antigen receptor signaling in a qualitative manner.

Publication types

  • Comparative Study
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Androstadienes / pharmacology
  • Animals
  • Antigens, CD19 / chemistry
  • Antigens, CD19 / genetics
  • Antigens, CD19 / physiology*
  • Binding Sites
  • Calcium / physiology*
  • DNA, Complementary / genetics
  • Enzyme Inhibitors / pharmacology
  • Extracellular Space / metabolism
  • Humans
  • Inositol 1,4,5-Trisphosphate / biosynthesis
  • Inositol 1,4,5-Trisphosphate / physiology*
  • Intracellular Fluid / metabolism
  • Mast-Cell Sarcoma / pathology
  • Mice
  • Mutagenesis, Site-Directed
  • Phosphatidylinositol 3-Kinases / physiology*
  • Phosphorylation / drug effects
  • Protein Processing, Post-Translational / drug effects
  • Protein-Tyrosine Kinases / antagonists & inhibitors
  • Receptors, Antigen, B-Cell / physiology*
  • Recombinant Fusion Proteins / physiology
  • Signal Transduction / physiology*
  • Spleen / cytology
  • Tumor Cells, Cultured
  • Wortmannin

Substances

  • Androstadienes
  • Antigens, CD19
  • DNA, Complementary
  • Enzyme Inhibitors
  • Receptors, Antigen, B-Cell
  • Recombinant Fusion Proteins
  • Inositol 1,4,5-Trisphosphate
  • Phosphatidylinositol 3-Kinases
  • Protein-Tyrosine Kinases
  • Calcium
  • Wortmannin