Gene expression signatures of circulating human type 1, 2, and 3 innate lymphoid cells

Li, Shuo; Morita, Hideaki; Sokołowska, Milena; Tan, Ge; Boonpiyathad, Tadech; Opitz, Lennart; Orimo, Keisuke; Archer, Stuart K.; Jansen, Kirstin; Tang, Mimi L.K.; Purcell, Damian F. J.; Plebanski, Magdalena; Akdiş, Cezmi A.

doi:10.1016/j.jaci.2019.01.047

Cited by 27 publications

(44 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Analysis of gene activities in primary ILCs was performed using public transcriptome dataset GSE112591 generated from purified ILC subsets which were isolated from the peripheral blood of healthy donors [30]. We found differential expression of several known ILC markers including cytokine and master factor encoding genes in addition to novel candidates in ILC1 (GZMB and TBX21, PRDM1), ILC2 (IL13 and GATA3, GFI1, LMO4), and ILC3 (CSF2 and TCF7, AHR, NFIL3, IL1R1, IL2RA, TIMP1, ID2, CARD19, BHLHE40), supporting the validity of these data (Supplementary Table 1, Supplementary Figure 1A-1C) [7].…”

Section: Ilc3 Express Nkl Homeobox Gene Hhexmentioning

confidence: 99%

“…Transcriptome data from primary ILCs were obtained from Gene Expression Omnibus (GEO; https://www.ncbi. nlm.nih.gov/gds) using datasets GSE112591, GSE124474 and GSE90834 and obtained from ArrayExpress (AE; https://www.ebi.ac.uk/) using dataset E-MTAB-8494 [30][31][32][33]. Expression values for each ILC type were averaged and listed in Supplementary Tables 1-4.…”

Section: Transcriptome Analysis Expression Profiling and Bioinformatmentioning

confidence: 99%

See 1 more Smart Citation

The NKL-code for innate lymphoid cells reveals deregulated expression of NKL homeobox genes HHEX and HLX in anaplastic large cell lymphoma (ALCL)

et al. 2020

View full text Add to dashboard Cite

NKL homeobox genes encode developmental transcription factors and display an NKL-code according to their physiological expression pattern in hematopoiesis. Here, we analyzed public transcriptome data from primary innate lymphoid cells (ILCs) for NKL homeobox gene activities and found that ILC3 expressed exclusively HHEX while in ILC1 and ILC2 these genes were silenced. Deregulation of the NKL-code promotes hematopoietic malignancies, including anaplastic large cell lymphoma (ALCL) which reportedly may derive from ILC3. Accordingly, we analyzed NKL homeobox gene activities in ALCL cell lines and investigated their role in this malignancy. Transcriptome analyses demonstrated low expression levels of HHEX but powerfully activated HLX. Forced expression of HHEX in ALCL cell lines induced genes involved in apoptosis and ILC3 differentiation, indicating tumor suppressor activity. ALCL associated NPM1-ALK and JAK-STAT3-signalling drove enhanced expression of HLX while discounting HHEX. Genomic profiling revealed copy number gains at the loci of HLX and STAT3 in addition to genes encoding both STAT3 regulators (AURKA,

show abstract

Section: Ilc3 Express Nkl Homeobox Gene Hhexmentioning

confidence: 99%

Section: Transcriptome Analysis Expression Profiling and Bioinformatmentioning

confidence: 99%

The NKL-code for innate lymphoid cells reveals deregulated expression of NKL homeobox genes HHEX and HLX in anaplastic large cell lymphoma (ALCL)

et al. 2020

View full text Add to dashboard Cite

show abstract

“…The transient receptor potential cation channel subfamily V member1 (TRPV1) is upregulated by ozone in experimental asthma, which is sensitive to a TRPV1 antagonist. The TRPV1 antagonist suppresses the neuropeptide calcitonin gene-related peptide (CGRP) and thymic stromal lymphopoietin (TSLP) (54). Thus, TRPV1 expression may be an important mechanism for asthma exacerbation upon exposure to ozone and other environmental pollutants.…”

Section: Airway Hyperreactivitymentioning

confidence: 99%

“…Thus, TRPV1 expression may be an important mechanism for asthma exacerbation upon exposure to ozone and other environmental pollutants. Ozone induced AHR and lung inflammation is characterized by increased neutrophils recruitment in the airways and lung (54), although the role of neutrophils in inducing AHR is controversial (55, 56). Interestingly, NKT cell-deficient (CD1d −/− and Jα18 −/− ) mice are resistant to ozone-induced AHR and have reduced neutrophils.…”

Section: Airway Hyperreactivitymentioning

confidence: 99%

See 1 more Smart Citation

Acute Respiratory Barrier Disruption by Ozone Exposure in Mice

et al. 2019

Self Cite

View full text Add to dashboard Cite

Ozone exposure causes irritation, airway hyperreactivity (AHR), inflammation of the airways, and destruction of alveoli (emphysema), the gas exchange area of the lung in human and mice. This review focuses on the acute disruption of the respiratory epithelial barrier in mice. A single high dose ozone exposure (1 ppm for 1 h) causes first a break of the bronchiolar epithelium within 2 h with leak of serum proteins in the broncho-alveolar space, disruption of epithelial tight junctions and cell death, which is followed at 6 h by ROS activation, AHR, myeloid cell recruitment, and remodeling. High ROS levels activate a novel PGAM5 phosphatase dependent cell-death pathway, called oxeiptosis. Bronchiolar cell wall damage and inflammation upon a single ozone exposure are reversible. However, chronic ozone exposure leads to progressive and irreversible loss of alveolar epithelial cells and alveoli with reduced gas exchange space known as emphysema. It is further associated with chronic inflammation and fibrosis of the lung, resembling other environmental pollutants and cigarette smoke in pathogenesis of asthma, and chronic obstructive pulmonary disease (COPD). Here, we review recent data on the mechanisms of ozone induced injury on the different cell types and pathways with a focus on the role of the IL-1 family cytokines and the related IL-33. The relation of chronic ozone exposure induced lung disease with asthma and COPD and the fact that ozone exacerbates asthma and COPD is emphasized.

show abstract

Distinct and shared gene expression for human innate versus adaptive helper lymphoid cells

Ercolano

Wyss

Salomé

et al. 2020

Journal of Leukocyte Biology

View full text Add to dashboard Cite

Innate lymphoid cells (ILCs) are the latest identified innate immune cell family. Given their similarity in transcription factor expression and cytokine secretion profiles, ILCs have been considered as the innate phenocopy of CD4 Th cells. Here, we explored the transcriptome of circulating human ILC subsets as opposed to CD4 Th cell subsets. We describe transcriptomic differences between total ILCs and total CD4 Th cells, as well as between paired innate and adaptive cell subsets (ILC1 vs. Th1; ILC2 vs. Th2; and ILC3 vs. Th17 cells). In particular, we observed differences in expression of genes involved in cell trafficking such as CCR1, CCR6 and CXCR3, innate activation and inhibitory functions, including CD119, 2B4, TIGIT, and CTLA-4, and neuropeptide receptors, such as VIPR2. Moreover, we report for the first time on distinct expression of long noncoding RNAs (lncRNAs) in innate vs. adaptive cells, arguing for a potential role of lncRNA in shaping human ILC biology. Altogether, our results point for unique, rather than redundant gene organization in ILCs compared to CD4 Th cells, in regard to kinetics, fine-tuning and spatial organization of the immune response.

show abstract

Gene expression signatures of circulating human type 1, 2, and 3 innate lymphoid cells

Abstract: and by the ''Angelo Nocivelli'' Foundation. Disclosure of potential conflict of interest: The authors declare that they have no relevant conflicts of interest.

Cited by 27 publications

References 9 publications

The NKL-code for innate lymphoid cells reveals deregulated expression of NKL homeobox genes HHEX and HLX in anaplastic large cell lymphoma (ALCL)

The NKL-code for innate lymphoid cells reveals deregulated expression of NKL homeobox genes HHEX and HLX in anaplastic large cell lymphoma (ALCL)

Acute Respiratory Barrier Disruption by Ozone Exposure in Mice

Distinct and shared gene expression for human innate versus adaptive helper lymphoid cells

Contact Info

Product

Resources

About