Regulation of the B cell response to T-dependent antigens by classical pathway complement

J Immunol. 1996 Jul 15;157(2):549-56.


Mice deficient in complement components C3 (C3 -/-) and C4 (C4 -/-) were found to have a profound defect in their Ab response to a T-dependent Ag (bacteriophage (phi X174). Characterization of the deficient mice demonstrated a diminished level of peanut agglutinin+ germinal centers and a failure in isotype switching despite normal B cell signaling in vitro. The nature of the defect was found to lie at the B cell level, as the T cells were primed in C3- and C4-deficient mice as well as those in wild-type mice. These results, and the finding that the defect could be partly reversed by a 10-fold increase in Ag dose, support the hypothesis that covalent attachment of complement ligands, i.e., C3b and C3d to the Ag-Ab complex, increases its immunogenicity.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antibodies, Viral / biosynthesis
  • Antigens, Viral / pharmacology
  • B-Lymphocytes / drug effects
  • B-Lymphocytes / immunology*
  • Bacteriophage phi X 174 / immunology
  • Complement C3 / deficiency
  • Complement C4 / deficiency
  • Complement Pathway, Classical*
  • Complement System Proteins / pharmacology*
  • Female
  • Germinal Center / immunology
  • Lymphocyte Activation / genetics
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Mutant Strains
  • Spleen / cytology
  • Spleen / immunology
  • T-Lymphocytes / immunology*


  • Antibodies, Viral
  • Antigens, Viral
  • Complement C3
  • Complement C4
  • Complement System Proteins