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The adaptive immune response, a sophisticated defense mechanism, relies on the activation and differentiation of B lymphocytes, or B cells. These processes enable our bodies to mount a tailored response against specific pathogens such as bacteria, free virus particles, toxins, and parasites.
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The adaptive immune system, a crucial component of the overall immune response, offers a highly specialized defense against pathogens. It involves specific cell types and features, enabling it to combat infections effectively and efficiently.
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Related Experiment Video

Updated: Mar 29, 2026

The Isolation, Differentiation, and Quantification of Human Antibody-secreting B Cells from Blood: ELISpot as a Functional Readout of Humoral Immunity
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IgG-Immune Complexes Promote B Cell Memory by Inducing BAFF.

SunAh Kang1, Amanda B Keener1, Shannon Z Jones2

  • 1Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599;

Journal of Immunology (Baltimore, Md. : 1950)
|December 2, 2015
PubMed
Summary

Early antibody responses involving IgG immune complexes (ICs) and Fc receptors promote B cell memory formation. This process relies on BAFF signaling, crucial for optimal immune memory against infections.

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Area of Science:

  • Immunology
  • Cellular and Molecular Immunology
  • Vaccinology

Background:

  • Memory B cell responses are critical for adaptive immunity and preventing reinfection.
  • Formation of high-affinity memory B cells requires T cell help, somatic hypermutation, and affinity maturation within germinal centers (GCs).
  • The specific signals committing GC B cells to the memory pool are not fully understood.

Purpose of the Study:

  • To investigate the role of IgG-immune complexes (ICs), Fc gamma receptors (FcγRs), and BAFF in memory B cell formation.
  • To elucidate the signaling pathways involved in the commitment of GC B cells to the memory pool.

Main Methods:

  • Immunization of mice with a T-dependent antigen.
  • Analysis of B cell populations, including germinal center (GC) and memory B cells.
  • In vivo manipulation involving genetic deletion (CD16) or blocking of IC:FcγR interactions.
  • Assessment of Bcl-6 expression and antibody responses.

Main Results:

  • Early IgG secretion formed immune complexes (ICs) that engaged FcγRs on dendritic cells.
  • This interaction induced dendritic cell secretion of BAFF, which acted on B cells to promote Bcl-6 expression.
  • Loss of FcγR signaling (CD16), BAFF, or IC:FcγR interactions impaired GC and memory B cell formation and secondary antibody responses.
  • BAFF also supported the maintenance/expansion of follicular helper T cells.

Conclusions:

  • Early antibody responses, mediated by IgG-ICs and FcγRs, are essential for optimal memory B cell formation.
  • BAFF signaling, induced by IC-FcγR interactions, plays a key role in this process, acting upstream or at Bcl-6.
  • This study identifies a novel role for FcγRs in regulating germinal center and memory B cell responses.