Dampening type 2 properties of group 2 innate lymphoid cells by a gammaherpesvirus infection reprograms alveolar macrophages.
In: Science Immunology, 8 (80), eabl9041 (2023-02-24, 2023
Online
academicJournal
Zugriff:
peer reviewed ; Immunological dysregulation in asthma is associated with changes in exposure to microorganisms early in life. Gammaherpesviruses (γHVs), such as Epstein-Barr virus, are widespread human viruses that establish lifelong infection and profoundly shape host immunity. Using murid herpesvirus 4 (MuHV-4), a mouse γHV, we show that after infection, lung-resident and recruited group 2 innate lymphoid cells (ILC2s) exhibit a reduced ability to expand and produce type 2 cytokines in response to house dust mites, thereby contributing to protection against asthma. In contrast, MuHV-4 infection triggers GM-CSF production by those lung ILC2s, which orders the differentiation of monocytes (Mos) into alveolar macrophages (AMs) without promoting their type 2 functions. In the context of γHV infection, ILC2s are therefore essential cells within the pulmonary niche that imprint the tissue-specific identity of Mo-derived AMs and shape their function well beyond the initial acute infection.
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Dampening type 2 properties of group 2 innate lymphoid cells by a gammaherpesvirus infection reprograms alveolar macrophages.
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Autor/in / Beteiligte Person: | Loos, Pauline ; Baiwir, Jérôme ; Maquet, Céline ; Javaux, Justine ; Sandor, Rémy ; LALLEMAND, François ; Marichal, Thomas ; Machiels, Bénédicte ; Gillet, Laurent |
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Zeitschrift: | Science Immunology, 8 (80), eabl9041 (2023-02-24, 2023 |
Veröffentlichung: | American Association for the Advancement of Science (AAAS), 2023 |
Medientyp: | academicJournal |
ISSN: | 2470-9468 (print) |
DOI: | 10.1126/sciimmunol.abl9041 |
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