Innate lymphoid cells in lung infection and immunity

Stehle, Christina; Hernandez, Daniela; Romagnani, Chiara

doi:10.1111/imr.12712

Cited by 42 publications

(54 citation statements)

References 200 publications

(322 reference statements)

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“…Despite only representing a minor fraction of total ILCs in the lung, 58,64 there is evidence that ILC1s play a role in immunosurveillance and infection control. Despite only representing a minor fraction of total ILCs in the lung, 58,64 there is evidence that ILC1s play a role in immunosurveillance and infection control.…”

Section: Innate Lymphoid Cellsmentioning

confidence: 99%

“…ILC1s and cytotoxic natural killer (NK) cells have shared developmental pathways and are considered to fall under the same immunological lineage 57 ; however, as NK cells have been long described and ILC1s are a relatively new player, here we will review cytotoxic ILC1s ('NK cells') and non-cytotoxic ILC1s (referred to as 'ILC1s') separately. Despite only representing a minor fraction of total ILCs in the lung, 58,64 there is evidence that ILC1s play a role in immunosurveillance and infection control. In mice infected with H1N1 influenza virus, ILC1s become activated and produce interferon-c (IFN-c) and tumour necrosis factor-a as early as day 3, suggesting a role in initiating the early response to infection; 65 and transfer of ILC1s to lymphocyte-deficient mice (Rag2 À/À cC À/À ), reduces viral titres in the lung.…”

Section: Ilc1smentioning

confidence: 99%

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Tissue‐resident innate immunity in the lung

2019

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The lung is a unique organ that must protect against inhaled pathogens and toxins, without mounting a disproportionate response against harmless particulate matter and without compromising its vital function. Tissue-resident immune cells within the lung provide local immunity and protection from infection but are also responsible for causing disease when dysregulated. There is a growing appreciation of the importance of tissue-resident memory T cells to lung immunity, but non-recirculating, tissue-resident, innate immune cells also exist. These cells provide the first line of defence against pulmonary infection and are essential for co-ordinating the subsequent adaptive response. In this review, we discuss the main lung-resident innate immune subsets and their functions in common pulmonary diseases, such as influenza, bacterial pneumonia, asthma and inflammatory disorders.

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Section: Innate Lymphoid Cellsmentioning

confidence: 99%

Section: Ilc1smentioning

confidence: 99%

Tissue‐resident innate immunity in the lung

2019

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“…In case of allergic or infectious lung diseases, inflammatory mediators like IL-33, IL-25, and thymic stromal lymphopoetin are locally released by damaged epithelial cells and potently stimulate ILC2 activity (30)(31)(32)(33)(34)(35). Mainly via the secretion of characteristic cytokines (e.g., IL-5, IL-13, IL-9, and IL-4) and growth factors, but also based on cell contact-dependent mechanisms, activated ILC2s promote type-2 immune responses, support mucosal wound healing and, thereby, crucially impact on the maintenance and reconstitution of tissue homeostasis (27,(36)(37)(38)(39)(40). Overwhelming ILC2 activation, however, was found to be involved in chronic inflammation, allergy, and fibrotic tissue remodeling (24,41,42).…”

Section: Introductionmentioning

confidence: 99%

ILC2 Lung-Homing in Cystic Fibrosis Patients: Functional Involvement of CCR6 and Impact on Respiratory Failure

et al. 2020

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Cystic fibrosis patients suffer from a progressive, often fatal lung disease, which is based on a complex interplay between chronic infections, locally accumulating immune cells and pulmonary tissue remodeling. Although group-2 innate lymphoid cells (ILC2s) act as crucial initiators of lung inflammation, our understanding of their involvement in the pathogenesis of cystic fibrosis remains incomplete. Here we report a marked decrease of circulating CCR6 + ILC2s in the blood of cystic fibrosis patients, which significantly correlated with high disease severity and advanced pulmonary failure, strongly implicating increased ILC2 homing from the peripheral blood to the chronically inflamed lung tissue in cystic fibrosis patients. On a functional level, the CCR6 ligand CCL20 was identified as potent promoter of lung-directed ILC2 migration upon inflammatory conditions in vitro and in vivo using a new humanized mouse model with light-sheet fluorescence microscopic visualization of lung-accumulated human ILC2s. In the lung, blood-derived human ILC2s were able to augment local eosinophil and neutrophil accumulation and induced a marked upregulation of pulmonary type-VI collagen expression. Studies in primary human lung fibroblasts additionally revealed ILC2-derived IL-4 and IL-13 as important mediators of this type-VI collagen-inducing effect. Taken together, the here acquired results suggest that pathologically increased CCL20 levels in cystic fibrosis airways induce CCR6-mediated lung homing of circulating human ILC2s. Subsequent ILC2 activation then triggers local production of type-VI collagen and might thereby drive extracellular matrix remodeling potentially influencing pulmonary tissue destruction in cystic fibrosis patients. Thus, modulating the lung homing capacity of circulating ILC2s and their local effector functions opens new therapeutic avenues for cystic fibrosis treatment.

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“…31 Moreover, NK cells rapidly produce a wide framework of IFN-γ and chemokines following stimulation by respiratory viral infections. 32…”

Section: Effector Phasementioning

confidence: 99%

Innate immune evasion by SARS‐CoV‐2: Comparison with SARS‐CoV

Bouayad

2020

Reviews in Medical Virology

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SARS-CoV-2 virus, a member of the Coronaviridae family, causes Covid-19 pandemic disease with severe respiratory illness. Multiple strategies enable SARS-CoV-2 to eventually overcome antiviral innate immune mechanisms which are important components of viral pathogenesis. This review considers several mechanisms of SARS-CoV-2 innate immune evasion including suppression of IFN-α/β production at the earliest stage of infection, mechanisms that exhaust natural killer cell-mediated cytotoxicity, overstimulation of NLRP3 inflammasome and induction of a cytokine storm. A comparison with SARS-CoV is made. Greater knowledge of these and other immune evasion tactics may provide us with improved possibilities for research into this novel deadly virus.

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Innate lymphoid cells in lung infection and immunity

Cited by 42 publications

References 200 publications

Tissue‐resident innate immunity in the lung

Tissue‐resident innate immunity in the lung

ILC2 Lung-Homing in Cystic Fibrosis Patients: Functional Involvement of CCR6 and Impact on Respiratory Failure

Innate immune evasion by SARS‐CoV‐2: Comparison with SARS‐CoV

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