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CR2 ligands modulate human B cell activation.

J F Bohnsack1, N R Cooper

  • 1Department of Immunology, Scripps Clinic, La Jolla, CA 92037.

Journal of Immunology (Baltimore, Md. : 1950)
|October 15, 1988
PubMed
Summary
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Complement receptor type 2 (CR2) ligands influence B cell growth by enhancing cell cycle transition. Monomeric C3dg inhibited activation, while aggregated forms and EBVUV promoted it in activated B cells.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Complement receptor type 2 (CR2) is known to modulate B cell activation and growth.
  • Understanding CR2's role requires investigating various ligand interactions with B cells.

Purpose of the Study:

  • To examine the effects of different CR2 ligands on highly purified, high-density resting tonsil B cells.
  • To elucidate the specific signals mediated by CR2 that influence B cell growth.

Main Methods:

  • Tested monomeric, aggregated, and latex-bound C3dg, anti-CR2 monoclonal antibodies (mAbs), and UV-inactivated Epstein-Barr virus (EBVUV) on resting tonsil B cells.
  • Assessed B cell activation, cell cycle entry, and thymidine incorporation in response to CR2 ligands, with or without co-stimuli like phorbol ester.

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Main Results:

  • CR2 ligands did not induce cell cycle entry or synergize with anti-mu or B cell growth factor for mitogenesis.
  • Aggregated C3dg, latex-bound C3dg, OKB7 anti-CR2 mAb, and EBVUV enhanced thymidine incorporation in phorbol ester-activated B cells, independent of T cells or monocytes.
  • Monomeric C3dg inhibited B cell activation, while the HB-5 anti-CR2 mAb did not synergize with PMA.

Conclusions:

  • CR2 ligands primarily enhance the transition of activated B cells from G1 to S phase.
  • Different forms of C3dg exert distinct effects on B cell activation.
  • These findings support a role for CR2 in controlling B cell growth and offer a model for studying CR2-mediated signals.