Innate immune cells in asthma

Deckers, Julie; Madeira, Filipe Branco; Hammad, Hamida

doi:10.1016/j.it.2013.08.004

Cited by 100 publications

(81 citation statements)

References 117 publications

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“…Although various mouse models of asthma have evidently demonstrated the significance of Th2 cells in monitoring the inflammatory responses in the lung, recent studies have indicated that innate immune cells also play a crucial role in allergic asthma [37]. Multiple cytokines, including IL-25, IL-33, and TSLP, produced by lung epithelial cells could induce the production of Th2 cell type cytokines and the infiltration of eosinophilic into lung tissues [38].…”

Section: Discussionmentioning

confidence: 99%

miR-146a Mimics Attenuate Allergic Airway Inflammation by Impacted Group 2 Innate Lymphoid Cells in an Ovalbumin-Induced Asthma Mouse Model

Han¹,

Ma²,

Bao³

et al. 2018

Int Arch Allergy Immunol

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Background: The prevalence of allergic asthma has increased dramatically. Previous studies have found that the microRNA 146a (miR-146a) expression in asthma inhibits cell proliferation and promotes apoptosis of bronchial smooth muscle cells. We aimed to investigate the effect of miR-146a mimics on ovalbumin (OVA)-induced asthma in a mouse model. Methods: Inflammatory cell infiltration in bronchoalveolar lavage fluid (BALF) was measured by flow cytometry. Levels of OVA-specific immunoglobulin E (IgE) in serum and cytokines in BALF were examined by enzyme-linked immunosorbent assay. For monitoring the airway, the Penh value (% baseline) was measured using a whole-body plethysmograph. Results: In OVA-induced asthmatic mice, miR-146a significantly suppressed the infiltration of inflammatory cells in BALF and decreased the levels of OVA-specific IgE and T helper 2 cell type cytokines. In addition, miR-146a inhibited the OVA-induced airway hyperresponsiveness and the group 2 innate lymphoid cell responses. Moreover, the effects of miR-146a mimics were dependent on interleukin 33 stimulation. Conclusions: Our results suggest that miR-146a mimics might serve as an attractive candidate for further preclinical studies as an anti-inflammatory treatment of asthma.

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Section: Discussionmentioning

confidence: 99%

miR-146a Mimics Attenuate Allergic Airway Inflammation by Impacted Group 2 Innate Lymphoid Cells in an Ovalbumin-Induced Asthma Mouse Model

Han¹,

Ma²,

Bao³

et al. 2018

Int Arch Allergy Immunol

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“…IgE synthesis is thought to occur through different biosynthetic pathways, either by "direct" class-switch recombination (CSR) from IgM, in germinal centre B-cells, or through "sequential" switch from IgM to IgG1 and then from IgG1 to IgE, which may occur outside of germinal centres. Although it is thought that IgE memory (of allergens) originally sits in IgG, it was shown that (human) blood or tonsil B-cells may undergo CSR to IgE upon CD40 ligation and activation by interleukin (IL)-4 or IL-13, produced by T-helper (Th) 2 cells, as well as also by the recently described type 2 innate lymphoid cells (ILC2) formerly referred to as "nuocytes" or "natural helper cells" [9][10][11]. These cells have similar morphological properties in common with lymphocytes, but lack the B-or T-cell receptor and lineage cell surface markers.…”

Section: Role Of Ige and Its Receptorsmentioning

confidence: 99%

Asthma phenotypes and IgE responses

et al. 2015

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The discovery of IgE represented a major breakthrough in allergy and asthma research, whereas the clinical interest given to IgE in asthma has been blurred until the arrival of anti-IgE biotherapy. Novel facets of the complex link between IgE and asthma have been highlighted by the effect of this treatment and by basic research. In parallel, asthma phenotyping recently evolved to the concept of endotypes, relying on identified/suspected pathobiological mechanisms to phenotype patients, but has not yet clearly positioned IgE among biomarkers of asthma.In this review, we first summarise recent knowledge about the regulation of IgE production and its main receptor, FcεRI. In addition to allergens acting as classical IgE inducers, viral infections as well as air pollution may trigger the IgE pathway, notably resetting the threshold of IgE sensitivity by regulating FcεRI expression. We then analyse the place of IgE in different asthma endo/phenotypes and discuss the potential interest of IgE among biomarkers in asthma. @ERSpublications We summarise regulation of IgE production, and discuss IgE in different asthma endo/ phenotypes and among biomarkers

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“…Nevertheless, the translation of findings to the human system remains to be determined. Furthermore, allergen binding to PRR on EC induces IL-1 secretion which triggers IL-25 and IL-33 secretion in an autocrine feedback mechanism [92]. Finally, different mechanisms are involved in the activation of ILC2s.…”

Section: Allergens Drive Ec To Activate Type 2 Innate Lymphoid Cellsmentioning

confidence: 99%

What makes an allergen?

Scheurer

Toda

Vieths

2015

Clin Experimental Allergy

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SummaryAllergic diseases are an immune disorder reacting to certain type of allergen(s). Remarkably only a small number of proteins of the plant and animal proteome act as allergens. Therefore, allergens have been clustered according to their common structural, biochemical and functional features. Evidence has accumulated that some allergens possess intrinsic adjuvant properties to stimulate the innate immunity. The adjuvant properties appear to contribute to the allergenicity of the respective proteins, namely the ability to cause allergic sensitization in susceptible subjects or allergic reactions in sensitized individuals. Here, we discuss how allergens interact with the innate immune cells, in particular dendritic cells and epithelial cells, via binding to pattern recognition receptors, exhibiting proteolytic activities and/or inducting type 2 innate lymphoid cells (ILC2), thereby contributing to the sensitization and development of allergic diseases.

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Innate immune cells in asthma

Cited by 100 publications

References 117 publications

miR-146a Mimics Attenuate Allergic Airway Inflammation by Impacted Group 2 Innate Lymphoid Cells in an Ovalbumin-Induced Asthma Mouse Model

miR-146a Mimics Attenuate Allergic Airway Inflammation by Impacted Group 2 Innate Lymphoid Cells in an Ovalbumin-Induced Asthma Mouse Model

Asthma phenotypes and IgE responses

What makes an allergen?

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