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Interferon-driven deletion of antiviral B cells at the onset of chronic infection

Fallet, Benedict
Narr, Kerstin
Ertuna, Yusuf I
Cornille, Karen
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Published in Science Immunology. 2016, vol. 1, no. 4
Abstract Inadequate antibody responses and perturbed B cell compartments represent hallmarks of persistent microbial infections, but the mechanisms whereby persisting pathogens suppress humoral immunity remain poorly defined. Using adoptive transfer experiments in the context of a chronic lymphocytic choriomeningitis virus (LCMV) infection of mice, we have documented rapid depletion of virus-specific B cells that coincided with the early type I interferon response to infection. We found that the loss of activated B cells was driven by type I interferon (IFN-I) signaling to several cell types including dendritic cells, T cells and myeloid cells. Intriguingly, this process was independent of B cell-intrinsic IFN-I sensing and resulted from biased differentiation of naïve B cells into short-lived antibody-secreting cells. The ability to generate robust B cell responses was restored upon IFN-I receptor blockade or, partially, when experimentally depleting myeloid cells or the IFN-I-induced cytokines interleukin 10 and tumor necrosis factor alpha. We have termed this IFN-I-driven depletion of B cells "B cell decimation". Strategies to counter "B cell decimation" should thus help us better leverage humoral immunity in the combat against persistent microbial diseases.
PMID: 27872905
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Article (Accepted version) (2.8 MB) - public document Free access
Research group La Sclérose en plaques (908)
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FALLET, Benedict et al. Interferon-driven deletion of antiviral B cells at the onset of chronic infection. In: Science immunology, 2016, vol. 1, n° 4. doi: 10.1126/sciimmunol.aah6817 https://archive-ouverte.unige.ch/unige:94180

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Deposited on : 2017-05-11

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