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Antibody Effector Functions Mediated by FcY-Receptors Are Compromised during Persistent Viral Infection
  • Andreas Wieland
  • Rangaiah Shashidharamurthy, Philadelphia College of Osteopathic Medicine
  • Alice Kamphorst
  • Jinhwan Han
  • Rachael Aubert
  • Biswa Choudhury
  • Sean Stowell
  • Junghwa Lee
  • George Punkosdy
  • et al.
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Summary T cell dysfunction is well documented during chronic viral infections but little is known about functional abnormalities in humoral immunity. Here we report that mice persistently infected with lymphocytic choriomeningitis virus (LCMV) exhibit a severe defect in Fcγ-receptor (FcγR)-mediated antibody effector functions. Using transgenic mice expressing human CD20, we found that chronic LCMV infection impaired the depletion of B cells with rituximab, an anti-CD20 antibody widely used for the treatment of B cell lymphomas. In addition, FcγR-dependent activation of dendritic cells by agonistic anti-CD40 antibody was compromised in chronically infected mice. These defects were due to viral antigen-antibody complexes and not the chronic infection per se, because FcγR-mediated effector functions were normal in persistently infected mice that lacked LCMV-specific antibodies. Our findings have implications for the therapeutic use of antibodies and suggest that high levels of pre-existing immune complexes could limit the effectiveness of antibody therapy in humans.

This article was published in Immunity, Volume 42, Issue 2, Pages 367-378.

The published version is available at

Copyright © 2015 Elsevier.

Citation Information
Andreas Wieland, Rangaiah Shashidharamurthy, Alice Kamphorst, Jinhwan Han, et al.. "Antibody Effector Functions Mediated by FcY-Receptors Are Compromised during Persistent Viral Infection" Immunity Vol. 42 Iss. 2 (2015) p. 367 - 378
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