A Role for CR2 in FDC-B Cell Interactions

  • D. Qin
  • J. Wu
  • G. F. Burton
  • A. K. Szakal
  • J. G. Tew
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 417)

Abstract

If animals lack C3 or if C3 is destroyed by cobra venom factor, antibody responses are dramatically depressed1–5. Treatment of animals with mAb against CR2 or CD19, which are part of the CD19, CR2 TAPA-1 complex on B cells, also result in dramatically depressed antibody responses6–8. Furthermore, if animals are treated with a soluble construct of CR2, which will bind C3 fragments, the ability to mount a humoral response is markedly suppressed’. In addition, a recent study of CR2 knockout mice revealed that B cell expression of CR2 is required for immune responses to T-dependent antigens9. Furthermore, complement markedly lowers the threshold at which B cells respond to antigen and this effect may be attributable to the co-ligation of CR2 to BCR via the association with C3b-associated antigen10,11. It is also known that cross-linking of CR2 on the B cell by multiple C3b fragments on a carrier renders B cells more easily stimulated by mitogens including anti-μ12,13. These results suggest that CR2 is associated with an important signaling mechanism which is involved when B cells proliferate and differentiate into antibody forming cells (AFC).

Keywords

Immune Complex None None Complement Receptor Follicular Dendritic Cell Costimulatory Signal 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 1997

Authors and Affiliations

  • D. Qin
    • 1
  • J. Wu
    • 1
  • G. F. Burton
    • 1
  • A. K. Szakal
    • 2
  • J. G. Tew
    • 1
  1. 1.Department of Microbiology and ImmunologyMedical College of Virginia Virginia Commonwealth UniversityRichmondUSA
  2. 2.Department of Anatomy, Division of ImmunobiologyMedical College of Virginia Virginia Commonwealth UniversityRichmondUSA

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