Transcriptional control of ILC identity

Korchagina, Anna A.; Shein, Sergey A.; Koroleva, Ekaterina P.; Tumanov, Alexei V.

doi:10.3389/fimmu.2023.1146077

Cited by 11 publications

(7 citation statements)

References 168 publications

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“…C1 was characterized by a gene expression profile found in both ILC2s (CCR9, CD24a) (48,49) and ILC3s (Il22, Klrb1b) (50, 51) (Fig. 3E), a transcriptional signature in line with observed plasticity among ILC populations (52). C5 was defined by an activated ILC2 gene signature (Gata3, Klrg1, Il5, Il13, Il1rl1) (20, 53) (Fig.…”

Section: Prenatal Inflammation Transcriptionally Enhances Lung Ilc2 H...mentioning

confidence: 81%

Prenatal inflammation reprograms hyperactive ILC2s that promote allergic lung inflammation and airway dysfunction

López,

Griffin,

Aguilar

et al. 2023

Preprint

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Allergic asthma is a chronic respiratory disease that initiates in early life, but causal mechanisms are poorly understood. Here we examined how prenatal inflammation shapes allergic asthma susceptibility by reprogramming lung immunity from early development. Induction of Type I interferon-mediated inflammation during development provoked expansion and hyperactivation of group 2 innate lymphoid cells (ILC2s) seeding the developing lung. Hyperactivated ILC2s produced increased IL-5 and IL-13, and were associated with acute Th2 bias, eosinophilia, and decreased Tregs in the lung. The hyperactive ILC2 phenotype was recapitulated by adoptive transfer of a fetal liver precursor following exposure to prenatal inflammation, indicative of developmental programming. Programming of ILC2 function and subsequent lung immune remodeling by prenatal inflammation led to airway dysfunction at baseline and in response to papain, indicating increased asthma susceptibility. Our data provide a link by which developmental programming of progenitors by early-life inflammation drives lung immune remodeling and asthma susceptibility through hyperactivation of lung-resident ILC2s.One Sentence SummaryPrenatal inflammation programs asthma susceptibility by inducing the production of hyperactivated ILC2s in the developing lung.

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Section: Prenatal Inflammation Transcriptionally Enhances Lung Ilc2 H...mentioning

confidence: 81%

Prenatal inflammation reprograms hyperactive ILC2s that promote allergic lung inflammation and airway dysfunction

López,

Griffin,

Aguilar

et al. 2023

Preprint

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“…Additionally, we obtained 292 genes associated with innate lymphoid cells from DisGeNet. Moreover, our analysis of additional studies revealed that BCL11B, BATF, RUNX3, and ZBTB46 are associated with lymphoid cell immune typing ( Korchagina et al, 2023 ).…”

Section: Methodsmentioning

confidence: 88%

Prediction of distinct populations of innate lymphoid cells by transcriptional profiles

Dong,

Du,

et al. 2023

Front. Genet.

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Innate lymphoid cells (ILCs) are a unique type of lymphocyte that differ from adaptive lymphocytes in that they lack antigen receptors, which primarily reside in tissues and are closely associated with fibers. Despite their plasticity and heterogeneity, identifying ILCs in peripheral blood can be difficult due to their small numbers. Accurately and rapidly identifying ILCs is critical for studying homeostasis and inflammation. To address this challenge, we collect single-cell RNA-seq data from 647 patients, including 26,087 transcripts. Background screening, Lasso analysis, and principal component analysis (PCA) are used to select features. Finally, we employ a deep neural network to classify lymphocytes. Our method achieved the highest accuracy compared to other approaches. Furthermore, we identified four genes that play a vital role in lymphocyte development. Adding these gene transcripts into model, we were able to increase the model’s AUC. In summary, our study demonstrates the effectiveness of using single-cell transcriptomic analysis combined with machine learning techniques to accurately identify congenital lymphoid cells and advance our understanding of their development and function in the body.

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“…ILCs lack specific antigen-specific receptors like T cell receptors (TCRs) or B cell receptors (BCRs), leading to their ability to respond quickly to stimuli, particularly cytokines. ILCs can be classified into three distinct functional groups, namely ILC1s, ILC2s, and ILC3, similar to the classification of CD4 + T cells, with each corresponding to Th1, Th2, and Th17 cells, respectively [ 125 ].…”

Section: Immunological Barriers By Innate Lymphoid Cellsmentioning

confidence: 99%

Physiological and immunological barriers in the lung

Kageyama,

Ito,

Tanaka

et al. 2024

Semin Immunopathol

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The lungs serve as the primary organ for respiration, facilitating the vital exchange of gases with the bloodstream. Given their perpetual exposure to external particulates and pathogens, they possess intricate protective barriers. Cellular adhesion in the lungs is robustly maintained through tight junctions, adherens junctions, and desmosomes. Furthermore, the pulmonary system features a mucociliary clearance mechanism that synthesizes mucus and transports it to the outside. This mucus is enriched with chemical barriers like antimicrobial proteins and immunoglobulin A (IgA). Additionally, a complex immunological network comprising epithelial cells, neural cells, and immune cells plays a pivotal role in pulmonary defense. A comprehensive understanding of these protective systems offers valuable insights into potential pathologies and their therapeutic interventions.

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Transcriptional control of ILC identity

Cited by 11 publications

References 168 publications

Prenatal inflammation reprograms hyperactive ILC2s that promote allergic lung inflammation and airway dysfunction

Prenatal inflammation reprograms hyperactive ILC2s that promote allergic lung inflammation and airway dysfunction

Prediction of distinct populations of innate lymphoid cells by transcriptional profiles

Physiological and immunological barriers in the lung

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