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

Machiels, Bénédicte; Dourcy, Mickaël; Xiao, Xue; Javaux, Justine; Mesnil, Claire; Sabatel, Catherine; Desmecht, Daniël; Lallemand, François; Martinive, Philippe; Hammad, Hamida; Guilliams, Martin; Dewals, Benjamin G; Vanderplasschen, Alain; Lambrecht, Bart N.; Bureau, Fabrice; Gillet, Laurent

doi:10.1038/ni.3857

Cited by 183 publications

(229 citation statements)

References 52 publications

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“…Moreover, it will be interesting to see whether any of the currently licenced or future vaccines has the potential to induce heterologous protection from viral infection as well as asthma. Recently, gammaherpesvirus infection was shown to induce regulatory monocytes, which prevented experimental asthma in mice [149]. erefore, heterologous innate immune stimulation with tolerogenic or T1 promoting adjuvants [14] might be utilised to induce allergen tolerance (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…Vaccination with self-amplifying mRNA (SAM®) (GlaxoSmithKline, London, UK) in lipid nanoparticles, encoding for conserved internal IV A proteins (nucleoprotein [NP] and/or matrix protein 1 [M1]), induced proliferation of NP-and M1-speci c CD4 + 1 cells as well as NP [147][148][149][150][151][152][153][154][155] -speci c CD8 + T cells in mice. All vaccinated mice survived hetero-subtypic IV A challenge [64].…”

Section: In Uenza Virus (Iv)mentioning

confidence: 99%

“…A Toll-like receptor 2 (TLR2)-agonist together with a split IV vaccine, but not vaccine alone, protected mice against homologous and heterologous virus challenge. Heterologous e ects were dependent on CD8 + T cells speci c for NP [147][148][149][150][151][152][153][154][155] [65]. e HA consists of the highly variable globular head domain, which is the main target of the antibody response, and the stalk/stem domain.…”

Section: In Uenza Virus (Iv)mentioning

confidence: 99%

“…According to the latter, less frequent exposure to pathogens in early life is associated with the development of allergies [148]. Protective e ects of bacteria or bacterial products on asthma development have been well characterized [148], but also viruses [149] as well as respira-tory viruses, including IV [150], were shown to protect mice from asthma. Correlates of protection are induction of T1 immune responses, e.g.…”

Section: Asthma/allergymentioning

confidence: 99%

“…by stimulation of innate immune receptors, such as Toll-like receptors [148,151]. Viral infections were shown to protect from asthma by induction of an natural killer T (NKT) cell subset [150] or monocytes with a regulatory phenotype [149].…”

Section: Asthma/allergymentioning

confidence: 99%

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Respiratory virus-induced heterologous immunity

2018

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Purpose: To provide current knowledge on respiratory virus-induced heterologous immunity (HI) with a focus on humoral and cellular cross-reactivity. Adaptive heterologous immune responses have broad implications on infection, autoimmunity, allergy and transplant immunology. A better understanding of the mechanisms involved might ultimately open up possibilities for disease prevention, for example by vaccination. Methods: A structured literature search was performed using Medline and PubMed to provide an overview of the current knowledge on respiratoryvirus induced adaptive HI. Results: In HI the immune response towards one antigen results in an alteration of the immune response towards a second antigen. We provide an overview of respiratory virus-induced HI, including viruses such as respiratory syncytial virus (RSV), rhinovirus (RV), coronavirus (CoV) and in uenza virus (IV). We discuss T cell receptor (TCR) and humoral cross-reactivity as mechanisms of HI involving those respiratory viruses. Topics covered include HI between respiratory viruses as well as between respiratory viruses and other pathogens. Newly developed vaccines, which have the potential Cite this as Pusch E, Renz H, Skevaki C. Respiratory virus-induced heterologous immunity -Part of the problem or part of the solution? Allergo J Int 2018; 27:79-96

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Section: Discussionmentioning

confidence: 99%

Section: In Uenza Virus (Iv)mentioning

confidence: 99%

Section: In Uenza Virus (Iv)mentioning

confidence: 99%

Section: Asthma/allergymentioning

confidence: 99%

Section: Asthma/allergymentioning

confidence: 99%

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Respiratory virus-induced heterologous immunity

2018

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Innate Immune Training Initiates Efferocytosis to Protect against Lung Injury

Kang,

Kim,

Lee

et al. 2024

Advanced Science

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Innate immune training involves myelopoiesis, dynamic gene modulation, and functional reprogramming of myeloid cells in response to secondary heterologous challenges. The present study evaluates whether systemic innate immune training can protect tissues from local injury. Systemic pretreatment of mice with β‐glucan, a trained immunity agonist, reduces the mortality rate of mice with bleomycin‐induced lung injury and fibrosis, as well as decreasing collagen deposition in the lungs. β‐Glucan pretreatment induces neutrophil accumulation in the lungs and enhances efferocytosis. Training of mice with β‐glucan results in histone modification in both alveolar macrophages (AMs) and neighboring lung epithelial cells. Training also increases the production of RvD1 and soluble mediators by AMs and efferocytes. Efferocytosis increases trained immunity in AMs by stimulating RvD1 release, thus inducing SIRT1 expression in neighboring lung epithelial cells. Elevated epithelial SIRT1 expression is associated with decreased epithelial cell apoptosis after lung injury, attenuating tissue damage. Further, neutrophil depletion dampens the effects of β‐glucan on macrophage accumulation, epigenetic modification in lung macrophages, epithelial SIRT1 expression, and injury‐mediated fibrosis in the lung. These findings provide mechanistic insights into innate immune training and clues to the potential ability of centrally trained immunity to protect peripheral organs against injury‐mediated disorders.

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Recruitment of hepatic macrophages from monocytes is independent of IL‐4Rα but is associated with ablation of resident macrophages in schistosomiasis

et al. 2019

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Alternatively activated Mϕs (AAMϕ) accumulate in hepatic granulomas during schistosomiasis and have been suggested to originate in the bone marrow. What is less understood is how these Mϕ responses are regulated after S. mansoni infection. Here, we investigated the role of IL-4 receptor α-chain (IL-4Rα)-signalling in the dynamics of liver Mϕ responses. We observed that IL-4Rα signalling was dispensable for the recruitment of Ly6C hi monocytes and for their conversion into F4/80 hi CD64 hi CD11b hi Mϕ. Moreover, while IL-4Rα provided an AAMϕ phenotype to liver F4/80 hi CD64 hi CD11b hi Mϕ that was associated with regulation of granuloma formation, it was dispensable for host survival. Resident F4/80 hi CD64 hi CD11b lo Mϕ did not upregulate the AAMϕ signature gene Ym1. Rather, resident Mϕ nearly disappeared by week 8 after infection and artificial ablation of resident Mϕ in CD169 DTR mice did not affect the response to S. mansoni infection. Interestingly, ablation of CD169 + cells in naive mice resulted in the accumulation of F4/80 hi CD64 hi CD11b hi Mϕ, which was amplified when ablation occurred during schistosomiasis. Altogether, our results suggest the ablation of resident KCs after S. mansoni infection to be associated with the recruitment and accumulation of F4/80 hi CD64 hi CD11b hi Mϕ with lyz2-dependent IL-4Rα contributing to the regulation of granuloma inflammation but being dispensable for host survival.Keywords: liver r monocytes r mouse model r Mϕ r schistosomiasis See accompanying Commentary by Rückerl and CookAdditional supporting information may be found online in the Supporting Information section at the end of the article. infected with Schistosoma mansoni develop a severe liver pathology with granulomatous inflammatory responses directed toward the parasite eggs. During chronic infections, type 2 inflammation in the liver results in fibrosis, which leads to portal hypertension, bleeding from collateral vessels and ultimately death [2][3][4]. Mϕ accumulate in the liver and are a key cellular component in granuloma formation and host protection [2,5].Mϕ are plastic cells that can be alternatively activated by IL-4 and IL-13 via the type I or type II IL-4 receptor, respectively [6].

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

Cited by 183 publications

References 52 publications

Respiratory virus-induced heterologous immunity

Respiratory virus-induced heterologous immunity

Innate Immune Training Initiates Efferocytosis to Protect against Lung Injury

Recruitment of hepatic macrophages from monocytes is independent of IL‐4Rα but is associated with ablation of resident macrophages in schistosomiasis

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