The role of receptors for complement in the induction of polyclonal B-cell proliferation and differentiation.

Published

Journal Article

A panel of monoclonal antibodies and ligands that bind to the CR1 or CR2 complement receptors of B cells has been used to investigate the role of these membrane molecules in regulating B-cell proliferation and differentiation. When CR2 was modulated from the surface of B cells by treatment with the HB-5 antibody and a secondary goat anti-mouse immunoglobulin antibody, Epstein-Barr virus-induced polyclonal B-cell proliferation and immunoglobulin production were inhibited by 83 and 90%, respectively. In contrast, modulation of other cell surface molecules, HB-2, B1, and the C3b receptor (CR1), or pretreatment of B cells with C3d,g (a CR2 ligand) or HB-5 antibody, alone minimally inhibited these responses. Neither the HB-5 antibody C3d,g, nor a monoclonal antibody (YZ-1) reactive with CR1 induced resting B cells to proliferate, nor did they alter anti-mu antibody-induced proliferation. Similarly, treatment with C3d,g or with the HB-5 or YZ-1 antibodies did not induce B cells to secrete immunoglobulin or affect pokeweed mitogen-induced plasma-cell formation. Whereas CR2 appears to be the functionally relevant receptor for Epstein-Barr virus on B cells, the effects of ligand interactions with CR1 and CR2 on normal B-cell proliferation or differentiation remain unidentified.

Full Text

Duke Authors

Cited Authors

  • Tedder, TF; Weis, JJ; Clement, LT; Fearon, DT; Cooper, MD

Published Date

  • January 1, 1986

Published In

Volume / Issue

  • 6 / 1

Start / End Page

  • 65 - 73

PubMed ID

  • 3485654

Pubmed Central ID

  • 3485654

Electronic International Standard Serial Number (EISSN)

  • 1573-2592

International Standard Serial Number (ISSN)

  • 0271-9142

Digital Object Identifier (DOI)

  • 10.1007/bf00915366

Language

  • eng