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

Published

Journal Article

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.

Full Text

Duke Authors

Cited Authors

  • Fischer, MB; Ma, M; Goerg, S; Zhou, X; Xia, J; Finco, O; Han, S; Kelsoe, G; Howard, RG; Rothstein, TL; Kremmer, E; Rosen, FS; Carroll, MC

Published Date

  • July 1996

Published In

Volume / Issue

  • 157 / 2

Start / End Page

  • 549 - 556

PubMed ID

  • 8752901

Pubmed Central ID

  • 8752901

Electronic International Standard Serial Number (EISSN)

  • 1550-6606

International Standard Serial Number (ISSN)

  • 0022-1767

Language

  • eng