Suppression of Fcγ-receptor-mediated antibody effector function during persistent viral infection.

Yamada DH, Elsaesser H, Lux A, Timmerman JM, Morrison SL, De La Torre JC, Nimmerjahn F, Brooks DG (2015)


Publication Status: Published

Publication Type: Journal article

Publication year: 2015

Journal

Book Volume: 42

Pages Range: 379-90

Journal Issue: 2

DOI: 10.1016/j.immuni.2015.01.005

Abstract

Understanding how viruses subvert host immunity and persist is essential for developing strategies to eliminate infection. T cell exhaustion during chronic viral infection is well described, but effects on antibody-mediated effector activity are unclear. Herein, we show that increased amounts of immune complexes generated in mice persistently infected with lymphocytic choriomeningitis virus (LCMV) suppressed multiple Fcγ-receptor (FcγR) functions. The high amounts of immune complexes suppressed antibody-mediated cell depletion, therapeutic antibody-killing of LCMV infected cells and human CD20-expressing tumors, as well as reduced immune complex-mediated cross-presentation to T cells. Suppression of FcγR activity was not due to inhibitory FcγRs or high concentrations of free antibody, and proper FcγR functions were restored when persistently infected mice specifically lacked immune complexes. Thus, we identify a mechanism of immunosuppression during viral persistence with implications for understanding effective antibody activity aimed at pathogen control.

Authors with CRIS profile

Involved external institutions

How to cite

APA:

Yamada, D.H., Elsaesser, H., Lux, A., Timmerman, J.M., Morrison, S.L., De La Torre, J.C.,... Brooks, D.G. (2015). Suppression of Fcγ-receptor-mediated antibody effector function during persistent viral infection. Immunity, 42(2), 379-90. https://doi.org/10.1016/j.immuni.2015.01.005

MLA:

Yamada, Douglas H., et al. "Suppression of Fcγ-receptor-mediated antibody effector function during persistent viral infection." Immunity 42.2 (2015): 379-90.

BibTeX: Download