Burst-enhancing role of the IgG membrane tail as a molecular determinant of memory

Nat Immunol. 2002 Feb;3(2):182-8. doi: 10.1038/ni752. Epub 2002 Jan 14.

Abstract

The basis of immune memory leading to heightened secondary antibody responses is a longstanding unanswered issue. Here we show that a single irreversible molecular change in the B cell antigen receptor, which is brought about by immunoglobulin M (IgM) to IgG isotype switching, is sufficient to greatly increase the extrafollicular proliferative burst of antigen-specific B cells. The unique membrane-spanning regions of IgG do not alter the T cell-dependent activation and proliferation of antigen-specific B cells in vivo, but markedly increase the number of progeny cells and plasmablasts that accumulate. These results establish a key molecular determinant of immunological memory and define an unexpected cellular basis by which it enhances the magnitude of secondary antibody responses.

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Antibody Affinity
  • Antibody Formation
  • B-Lymphocytes / immunology*
  • Immunization, Secondary
  • Immunoglobulin Class Switching*
  • Immunoglobulin G / biosynthesis
  • Immunoglobulin Isotypes / biosynthesis*
  • Immunoglobulin M / biosynthesis
  • Immunologic Memory*
  • Lymphocyte Activation
  • Mice
  • Mice, Transgenic
  • Molecular Sequence Data
  • Muramidase / immunology
  • Receptors, Antigen, B-Cell / biosynthesis*
  • Spleen / cytology
  • Spleen / immunology

Substances

  • Immunoglobulin G
  • Immunoglobulin Isotypes
  • Immunoglobulin M
  • Receptors, Antigen, B-Cell
  • Muramidase