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A gammaherpesvirus provides protection against allergic asthma by inducing the replacement of resident alveolar macrophages with regulatory monocytes.

Authors
  • Machiels, Bénédicte1
  • Dourcy, Mickael1
  • Xiao, Xue1
  • Javaux, Justine1
  • Mesnil, Claire2
  • Sabatel, Catherine2
  • Desmecht, Daniel3
  • Lallemand, François4
  • Martinive, Philippe4
  • Hammad, Hamida5
  • Guilliams, Martin5
  • Dewals, Benjamin1
  • Vanderplasschen, Alain1
  • Lambrecht, Bart N5, 6
  • Bureau, Fabrice2
  • Gillet, Laurent1
  • 1 Immunology-Vaccinology, Department of Infectious and Parasitic Diseases, Faculty of Veterinary Medicine - FARAH, University of Liège, Liège, Belgium. , (Belgium)
  • 2 Cellular and Molecular Immunology, Department of Functional Sciences, Faculty of Veterinary Medicine - GIGA, University of Liège, Liège, Belgium. , (Belgium)
  • 3 Department of Pathology, Faculty of Veterinary Medicine - FARAH, University of Liège, Liège, Belgium. , (Belgium)
  • 4 Department of Radiology, University Hospital Liège, Liège, Belgium. , (Belgium)
  • 5 VIB Center for Inflammation Research, Ghent University, Ghent, Belgium. , (Belgium)
  • 6 Department of Pulmonary Medicine, Erasmus Medical Center, Rotterdam, the Netherlands. , (Netherlands)
Type
Published Article
Journal
Nature Immunology
Publisher
Springer Nature
Publication Date
Dec 01, 2017
Volume
18
Issue
12
Pages
1310–1320
Identifiers
DOI: 10.1038/ni.3857
PMID: 29035391
Source
Medline
License
Unknown

Abstract

The hygiene hypothesis postulates that the recent increase in allergic diseases such as asthma and hay fever observed in Western countries is linked to reduced exposure to childhood infections. Here we investigated how infection with a gammaherpesvirus affected the subsequent development of allergic asthma. We found that murid herpesvirus 4 (MuHV-4) inhibited the development of house dust mite (HDM)-induced experimental asthma by modulating lung innate immune cells. Specifically, infection with MuHV-4 caused the replacement of resident alveolar macrophages (AMs) by monocytes with regulatory functions. Monocyte-derived AMs blocked the ability of dendritic cells to trigger a HDM-specific response by the TH2 subset of helper T cells. Our results indicate that replacement of embryonic AMs by regulatory monocytes is a major mechanism underlying the long-term training of lung immunity after infection.

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