Group 2 innate lymphoid cells in nasal polyposis

Stevens, Whitney W.; Kato, Atsushi

doi:10.1016/j.anai.2020.08.001

Cited by 28 publications

(25 citation statements)

References 65 publications

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“…κB locus of the corresponding target gene to promote the transcription of the gene, resulting in a series of inflammatory reactions. In this study, pairwise comparisons did not show significant differences in the average methylation level of NFAT5 and the methylation levels at individual CpG loci among the three groups, which does not suggest a direct association of NFAT5 methylation with SRA [23].…”

Section: Discussioncontrasting

confidence: 78%

Associations of the Methylation Levels of NFAT5, PVT1, RPS6KA1, and MIB1 with Steroid-Resistant Asthma

Chen¹,

Wang²,

Leng³

et al. 2022

Int Arch Allergy Immunol

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Background: This study detected the methylation levels of nuclear factor-5 (NFAT5), PVT1, ribosomal protein S6 kinase A-1 (RPS6KA1), and MIB1 in patients with steroid-resistant asthma (SRA) and explored their associations with SRA. Methods: In our pilot study, we found abnormal methylation of NFAT5, PVT1, RPS6KA1, and MIB1 in SRA patients according to genome-wide methylation screening. This study expanded the sample size to further validate the results of the pilot study. Twenty patients with SRA, 20 patients with bronchial asthma, and 20 healthy volunteers constituted the SRA group, asthma control group, and healthy control group, respectively. The clinical data of all the participants were collected. Peripheral blood was taken for DNA extraction. The methylation loci and levels of NFAT5, PVT1, RPS6KA1, and MIB1 were detected using the Sequenom MassARRAY Nanodispenser RS1000. Data were processed and analyzed with SPSS 22.0 software. Results: There were 24 CpG loci detected in the NFAT5 segment 7 in the PVT1 segment, 4 in the RPS6KA1 segment, and 3 in the MIB1 segment. Among these genes, RPS6KA exhibited hypomethylation in the SRA group, which showed significant differences at the CpG_1, CpG_2, and CpG_3 loci compared with the other groups (p < 0.05). No significant differences in the methylation levels of NFAT5, PVT1, and MIB1 were observed among the groups (p > 0.05). Conclusions: RPS6KA1 is hypomethylated in SRA patients, which may play a role in the development of SRA via the MAPK signaling pathway. However, the influence of the methylation of NFAT5, PVT1, and MIB1 on SRA development remains to be explored.

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Section: Discussioncontrasting

confidence: 78%

Associations of the Methylation Levels of NFAT5, PVT1, RPS6KA1, and MIB1 with Steroid-Resistant Asthma

Chen¹,

Wang²,

Leng³

et al. 2022

Int Arch Allergy Immunol

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“…Besides their before described crucial involvement in the immunological responses directed against lung tissue-affecting infectious pathogens, ILC2s also represent important cellular modulators of non-infectious chronic inflammatory and fibrotic diseases of the upper and lower airways. Here we will in particular discuss the disease-modifying influence of local ILC2 pools on the pathogenesis of asthma, cystic fibrosis and idiopathic pulmonary fibrosis, but reference should also be made to the role of these cells in the course of inflammatory disorders of the upper airway such as chronic rhinosinusitis with nasal polyps, which has been extensively summarized by other review articles ( 81 , 82 ).…”

Section: Ilc2s As Drivers Of Human Chronic Lung Diseasesmentioning

confidence: 99%

Functional Contribution and Targeted Migration of Group-2 Innate Lymphoid Cells in Inflammatory Lung Diseases: Being at the Right Place at the Right Time

2021

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During the last decade, group-2 innate lymphoid cells (ILC2s) have been discovered and successfully established as crucial mediators of lung allergy, airway inflammation and fibrosis, thus affecting the pathogenesis and clinical course of many respiratory diseases, like for instance asthma, cystic fibrosis and chronic rhinosinusitis. As an important regulatory component in this context, the local pulmonary milieu at inflammatory tissue sites does not only determine the activation status of lung-infiltrating ILC2s, but also influences their motility and migratory behavior. In general, many data collected in recent murine and human studies argued against the former concept of a very strict tissue residency of innate lymphoid cells (ILCs) and instead pointed to a context-dependent homing capacity of peripheral blood ILC precursors and the inflammation-dependent capacity of specific ILC subsets for interorgan trafficking. In this review article, we provide a comprehensive overview of the so far described molecular mechanisms underlying the pulmonary migration of ILC2s and thereby the numeric regulation of local ILC2 pools at inflamed or fibrotic pulmonary tissue sites and discuss their potential to serve as innovative therapeutic targets in the treatment of inflammatory lung diseases.

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“…Although the mechanisms involved in proliferation and activation of ILC2s in CRS are not fully understood, mediators known to activate ILC2s (Fig 2 ), including TSLP, IL-4, IL-13, and various lipid mediators, are elevated in nasal polyps compared with healthy sinonasal tissues. 150 The levels of other ILC2 activators, such as IL-25 and IL-33, are rather controversial. 151 Recently, receptor activator of NF-kB (RANK) ligand (RANK-L, TNFSF11) was found to be elevated in nasal polyps.…”

Section: Chronic Rhinosinusitismentioning

confidence: 99%

Continuing Medical Education Calendar

2021

Journal of Allergy and Clinical Immunology

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In the 12 years since the discovery of innate lymphoid cells (ILCs), our knowledge of their immunobiology has expanded rapidly. Group 2 ILCs (ILC2s) respond rapidly to allergen exposure and environmental insults in mucosal organs, producing type 2 cytokines. Early studies showed that epithelium-derived cytokines activate ILC2s, resulting in eosinophilia, mucus hypersecretion, and remodeling of mucosal tissues. We now know that ILC2s are regulated by other cytokines, eicosanoids, and neuropeptides as well, and interact with both immune and stromal cells. Furthermore, ILC2s exhibit plasticity by adjusting their functions depending on their tissue environment and may consist of several heterogeneous subpopulations. Clinical studies show that ILC2s are involved in asthma, allergic rhinitis, chronic rhinosinusitis, food allergy, and eosinophilic esophagitis. However, much remains unknown about the immunologic mechanisms involved. Beneficial functions of ILCs in maintenance or restoration of tissue wellbeing and human health also need to be clarified. As our understanding of the crucial functions ILCs play in both homeostasis and disease pathology expands, we are poised to make tremendous strides in diagnostic and therapeutic options for patients with allergic diseases. This review summarizes discoveries in immunobiology of ILCs and their roles in allergic diseases in the past 5 years, discusses controversies and gaps in our knowledge, and suggests future research directions. (J

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Group 2 innate lymphoid cells in nasal polyposis

Cited by 28 publications

References 65 publications

Associations of the Methylation Levels of NFAT5, PVT1, RPS6KA1, and MIB1 with Steroid-Resistant Asthma

Associations of the Methylation Levels of NFAT5, PVT1, RPS6KA1, and MIB1 with Steroid-Resistant Asthma

Functional Contribution and Targeted Migration of Group-2 Innate Lymphoid Cells in Inflammatory Lung Diseases: Being at the Right Place at the Right Time

Continuing Medical Education Calendar

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