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APOBEC3 enzymes restrict marginal zone B cells.

Gabriele B Beck-Engeser1, Rebecca Winkelmann, Matthew L Wheeler

  • 1Department of Microbiology and Immunology, University of California, San Francisco, CA, USA.

European Journal of Immunology
|December 16, 2014
PubMed
Summary
This summary is machine-generated.

The enzyme Apobec3 (A3) influences viral immunity by altering B cell populations. A3 shifts immune responses from rapid, low-affinity antibody production to sustained, high-affinity responses for better viral neutralization.

Keywords:
Apobec3B cellHitchhiker-1Recovery from Friend virus 3 (Rfv3)Sialyl transferases

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Area of Science:

  • Immunology
  • Virology
  • Genetics

Background:

  • Long-lasting antiviral immunity typically requires infectious, replication-competent viruses.
  • The enzyme Apobec3 (A3) is known to control viremia before adaptive immune responses develop.
  • A3's role in adaptive immunity, particularly antibody response, is counterintuitive and warrants further investigation.

Purpose of the Study:

  • To investigate the impact of Apobec3 (A3) activity on adaptive immune cell populations.
  • To understand how A3 influences the development of neutralizing antibody responses against viruses.
  • To explore the relationship between A3, retroelements, and immune cell dynamics.

Main Methods:

  • Generated transgenic mice expressing human Apobec3 (A3) enzymes.
  • Compared immune cell populations in transgenic, wild-type (WT), and A3-deficient mice.
  • Analyzed gene expression, including retroelements and sialyl transferases, in A3-deficient mice.

Main Results:

  • Apobec3 (A3) enzymes reduced the number of marginal zone B cells.
  • A3 activity did not significantly affect follicular B or T cell populations.
  • Knockout of mouse A3 led to significant overexpression of hitchhiker-1 retroelements and sialyl transferases.

Conclusions:

  • Apobec3 (A3) modulates the immune response balance.
  • A3 shifts the immune system from rapid, low-affinity antibody responses (marginal zone B cells) to sustained, high-affinity responses (germinal center B cells).
  • This shift driven by A3 enhances the development of effective neutralizing antibodies against viral infections.