Innate Lymphoid Cells in Airway Inflammation

Pasha, M. Asghar; Yang, Qi

doi:10.1007/978-3-030-63046-1_11

Cited by 5 publications

(3 citation statements)

References 63 publications

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“…It is well appreciated that HDM exposure induces IL-33 production from epithelial cells, which induces eosinophilia in allergic asthma, 31 in particular via activation of ILC2. 48,49 We observed high concentrations of the C5aR1 ligand C5a in the BAL of HDM-or IL-33 treated mice, in line with previous reports. 32 Intriguingly, we found high intracellular and extracellular C5aR1 as well as C5 expression in iEOS, which was significantly higher than in rEOS.…”

Section: Discussionsupporting

confidence: 91%

“…Our data identified C5aR1 activation as a critical driver of pulmonary iEOS recruitment after one‐time but not after repeated HDM exposure, which is mainly driven by Th2 cells. It is well appreciated that HDM exposure induces IL‐33 production from epithelial cells, which induces eosinophilia in allergic asthma, 31 in particular via activation of ILC2 48,49 . We observed high concentrations of the C5aR1 ligand C5a in the BAL of HDM‐ or IL‐33 treated mice, in line with previous reports 32 .…”

Section: Discussionsupporting

confidence: 91%

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C5aR1 activation in mice controls inflammatory eosinophil recruitment and functions in allergic asthma

Wiese

Duhn

Korkmaz

et al. 2023

Allergy

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Background Pulmonary eosinophils comprise at least two distinct populations of resident eosinophils (rEOS) and inflammatory eosinophils (iEOS), the latter recruited in response to pulmonary inflammation. Here, we determined the impact of complement activation on rEOS and iEOS trafficking and function in two models of pulmonary inflammation. Methods BALB/c wild‐type and C5ar1−/− mice were exposed to different allergens or IL‐33. Eosinophil populations in the airways, lung, or mediastinal lymph nodes (mLN) were characterized by FACS or immunohistochemistry. rEOS and iEOS functions were determined in vivo and in vitro. Results HDM and IL‐33 exposure induced a strong accumulation of iEOS but not rEOS in the airways, lungs, and mLNs. rEOS and iEOS expressed C3/C5 and C5aR1, which were significantly higher in iEOS. Initial pulmonary trafficking of iEOS was markedly reduced in C5ar1−/− mice and associated with less IL‐5 production from ILC2 cells. Functionally, adoptively transferred pulmonary iEOS from WT but not from C5ar1−/− mice‐induced airway hyperresponsiveness (AHR), which was associated with significantly reduced C5ar1−/− iEOS degranulation. Pulmonary iEOS but not rEOS were frequently associated with T cells in lung tissue. After HDM or IL‐33 exposure, iEOS but not rEOS were found in mLNs, which were significantly reduced in C5ar1−/− mice. C5ar1−/− iEOS expressed less costimulatory molecules, associated with a decreased potency to drive antigen‐specific T cell proliferation and differentiation into memory T cells. Conclusions We uncovered novel roles for C5aR1 in iEOS trafficking and activation, which affects key aspects of allergic inflammation such as AHR, ILC2, and T cell activation.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 91%

C5aR1 activation in mice controls inflammatory eosinophil recruitment and functions in allergic asthma

Wiese

Duhn

Korkmaz

et al. 2023

Allergy

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“…Of the ILCs, ILC2s generate a type 2 property by producing type 2 cytokines. While they initiate allergic inflammation, such as lung asthma [73], recent studies have revealed that ILC2s effectively attenuate arthritis [69]. The induction of IL-4/IL-5/IL-13(+) ILC2s mitigated arthritis, suggesting the inflammation is regulated by ILC2s.…”

Section: Type 2 Innate Lymphoid Cells In Arthritismentioning

confidence: 99%

Inflammatory Arthritis and Bone Metabolism Regulated by Type 2 Innate and Adaptive Immunity

Omata

Frech

Saito

et al. 2022

IJMS

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While type 2 immunity has traditionally been associated with the control of parasitic infections and allergic reactions, increasing evidence suggests that type 2 immunity exerts regulatory functions on inflammatory diseases such as arthritis, and also on bone homeostasis. This review summarizes the current evidence of the regulatory role of type 2 immunity in arthritis and bone. Key type 2 cytokines, like interleukin (IL)-4 and IL-13, but also others such as IL-5, IL-9, IL-25, and IL-33, exert regulatory properties on arthritis, dampening inflammation and inducing resolution of joint swelling. Furthermore, these cytokines share anti-osteoclastogenic properties and thereby reduce bone resorption and protect bone. Cellular effectors of this action are both T cells (i.e., Th2 and Th9 cells), but also non-T cells, like type 2 innate lymphoid cells (ILC2). Key regulatory actions mediated by type 2 cytokines and immune cells on both inflammation as well as bone homeostasis are discussed.

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Penicilazaphilone C alleviates allergic airway inflammation and improves the immune microenvironment by hindering the NLRP3 inflammasome

Fu,

Huang,

Dai

et al. 2024

Biomedicine & Pharmacotherapy

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Innate Lymphoid Cells in Airway Inflammation

Cited by 5 publications

References 63 publications

C5aR1 activation in mice controls inflammatory eosinophil recruitment and functions in allergic asthma

C5aR1 activation in mice controls inflammatory eosinophil recruitment and functions in allergic asthma

Inflammatory Arthritis and Bone Metabolism Regulated by Type 2 Innate and Adaptive Immunity

Penicilazaphilone C alleviates allergic airway inflammation and improves the immune microenvironment by hindering the NLRP3 inflammasome

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