IgE cross-linking impairs monocyte antiviral responses and inhibits influenza-driven TH1 differentiation

Rowe, Regina K.; Pyle, David M.; Tomlinson, Andrew R.; Lv, Tinghong; Hu, Zizhong; Gill, Michelle A.

doi:10.1016/j.jaci.2016.11.035

Cited by 11 publications

(37 citation statements)

References 46 publications

(9 reference statements)

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“…1B). Similar to our previous findings with influenza (12), the strong Th1 response induced by RV-exposed monocytes was inhibited by IgE crosslinking (Supp. Fig.…”

Section: Ige-mediated Allergic Stimulation Enhances Rv-induced Monocysupporting

confidence: 90%

“…We previously established a model of monocyte-driven T cell development to evaluate the effects of IgE-mediated allergic stimulation on monocyte-driven T cell priming (12) observed with RV exposure alone ( Fig. 1B).…”

Section: Ige-mediated Allergic Stimulation Enhances Rv-induced Monocymentioning

confidence: 99%

“…Monocytes are antigen presenting cells (APCs) recruited to the airway during respiratory virus infections (9,10) and following allergen challenge (11), whose functions are modulated by the allergic environment (12)(13)(14)(15). Several studies indicate roles for monocytes and monocytederived cells in RV-induced allergic disease pathogenesis.…”

mentioning

confidence: 99%

“…In asthmatic subjects, experimental RVinfection resulted in exaggerated recruitment of monocytes/macrophages to the airways compared with control subjects which correlated with virus load (9). Our group has shown that IgE crosslinking induces monocyte secretion of regulatory and pro-inflammatory cytokines, including IL-10, IL-6, and tumor necrosis factor (TNF) a (12,13). IL-10 has been specifically linked to allergic disease pathogenesis and virus-induced wheezing (16)(17)(18), although its role in IgEmediated monocyte antiviral responses remains unexplored.…”

mentioning

confidence: 99%

“…IL-10 has been specifically linked to allergic disease pathogenesis and virus-induced wheezing (16)(17)(18), although its role in IgEmediated monocyte antiviral responses remains unexplored. We recently demonstrated that critical monocyte antiviral functions, including influenza-induced upregulation of antigen-presenting molecules and CD4 Th1 T cell priming are inhibited by IgE crosslinking (12). IgE-mediated regulation of monocyte functions during RV infection may thus play a role in promoting allergic inflammation.…”

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confidence: 99%

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IgE-mediated regulation of IL-10 and type I interferon enhances rhinovirus-induced Th2 priming by primary human monocytes

et al. 2018

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Rhinovirus infections are linked to the development and exacerbation of allergic diseases including allergic asthma. IgE, another contributor to atopic disease pathogenesis, has been shown to regulate dendritic cell antiviral functions and influence T cell priming by monocytes. We previously demonstrated that IgE-mediated stimulation of monocytes alters multiple cellular functions including cytokine secretion, phagocytosis, and influenza-induced Th1 priming. In this study, we investigate the effects of IgE-mediated allergic stimulation on monocyte-driven, RV-induced T cell priming utilizing primary human monocyte-T cell co-cultures. We demonstrate that IgE crosslinking of RV-exposed monocytes enhances monocyte-driven Th2 priming. This increase in RV-induced Th2 differentiation was regulated by IgE-mediated inhibition of type I interferon and induction of IL-10. These findings suggest an additional mechanism by which two clinically significant risk factors for allergic disease exacerbations – IgE-mediated stimulation and rhinovirus infection, may synergistically promote Th2 differentiation and allergic inflammation.

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“…1B). Similar to our previous findings with influenza (12), the strong Th1 response induced by RV-exposed monocytes was inhibited by IgE crosslinking (Supp. Fig.…”

Section: Ige-mediated Allergic Stimulation Enhances Rv-induced Monocysupporting

confidence: 90%

Section: Ige-mediated Allergic Stimulation Enhances Rv-induced Monocymentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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IgE-mediated regulation of IL-10 and type I interferon enhances rhinovirus-induced Th2 priming by primary human monocytes

et al. 2018

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IgE‐mediated regulation of IL‐10 and type I IFN enhances rhinovirus‐induced Th2 differentiation by primary human monocytes

et al. 2020

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Rhinovirus (RV) infections are linked to the development and exacerbation of allergic diseases including allergic asthma. IgE, another contributor to atopic disease pathogenesis, has been shown to regulate DC antiviral functions and influence T cell priming by monocytes. We previously demonstrated that IgE-mediated stimulation of monocytes alters multiple cellular functions including cytokine secretion, phagocytosis, and influenzainduced Th1 development. In this study, we investigate the effects of IgE-mediated stimulation on monocyte-driven, RV-induced T cell development utilizing primary human monocyte-T cell co-cultures. We demonstrate that IgE crosslinking of RV-exposed monocytes enhances monocyte-driven Th2 differentiation. This increase in RV-induced Th2 development was regulated by IgE-mediated inhibition of virus-induced type I IFN and induction of IL-10. These findings suggest an additional mechanism by which two clinically significant risk factors for allergic disease exacerbations-IgE-mediated stimulation and rhinovirus infection-may synergistically promote Th2 differentiation and allergic inflammation.

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Effects of Allergic Sensitization on Antiviral Immunity: Allergen, Virus, and Host Cell Mechanisms

Rowe

Gill

2017

Curr Allergy Asthma Rep

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Recent studies have focused on the molecular pathways and genetic influences involved in allergen-mediated inhibition of innate antiviral immune responses. Multiple tissue and cell types from atopic individuals across the atopy spectrum exhibit deficient interferon responses to a variety of virus infections. Impairment in barrier function, viral RNA and DNA recognition by intracellular sensing molecules, and dysregulation of signaling components are broadly affected by allergic sensitization. Finally, genetic predisposition by numerous nucleotide polymorphisms also impacts immune pathways and potentially contributes to virus-associated atopic disease pathogenesis. Allergen-virus interactions in the setting of atopy involve complex tissue and cellular mechanisms. Future studies defining the pathways underlying these interactions could uncover potential therapeutic targets. Available data suggest that therapies tailored to restore specific components of antiviral responses will likely lead to improved clinical outcomes in allergic disease.

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IgE cross-linking impairs monocyte antiviral responses and inhibits influenza-driven TH1 differentiation

Cited by 11 publications

References 46 publications

IgE-mediated regulation of IL-10 and type I interferon enhances rhinovirus-induced Th2 priming by primary human monocytes

IgE-mediated regulation of IL-10 and type I interferon enhances rhinovirus-induced Th2 priming by primary human monocytes

IgE‐mediated regulation of IL‐10 and type I IFN enhances rhinovirus‐induced Th2 differentiation by primary human monocytes

Effects of Allergic Sensitization on Antiviral Immunity: Allergen, Virus, and Host Cell Mechanisms

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