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| Status |
Public on Oct 06, 2023 |
| Title |
IL-33 priming and antigenic stimulation synergistically promote the transcription of proinflammatory cytokine and chemokine genes in human skin mast cells [ATAC-Seq] |
| Organism |
Homo sapiens |
| Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
|
| Summary |
Antigenic stimulation through cross-linking the IgE receptor and epithelial cell-derived cytokine IL-33 are potent stimuli of mast cell (MC) activation. Moreover, IL-33 primes a variety of cell types, including MCs to respond more vigorously to external stimuli. However, target genes induced by the combined IL-33 priming and antigenic stimulation have not been investigated in human skin mast cells (HSMCs) in a genome-wide manner. Furthermore, epigenetic changes induced by the combined IL-33 priming and antigenic stimulation have not been evaluated. In this study, we found that IL-33 priming of HSMCs enhanced their capacity to promote transcriptional synergy of the IL1B and CXCL8 genes by 16- and 3-fold, respectively, in response to combined IL-33 and antigen stimulation compared to without IL-33 priming. We identified the target genes in IL-33-primed HSMCs in response to the combined IL-33 and antigenic stimulation using RNA sequencing (RNA-seq). We found that the majority of genes synergistically upregulated in the IL-33-primed HSMCs in response to the combined IL-33 and antigenic stimulation were predominantly proinflammatory cytokine and chemokine genes. Moreover, the combined IL-33 priming and antigenic stimulation increase chromatin accessibility in the synergy target genes but not synergistically. Transcription factor binding motif analysis revealed more binding sites for NF-κB, AP-1, GABPA, and RAP1 in the induced or increased chromatin accessible regions of the synergy target genes. Our study demonstrates that IL-33 priming greatly potentiates MCs’ ability to transcribe proinflammatory cytokine and chemokine genes in response to antigenic stimulation, shining light on how epithelial cell-derived cytokine IL-33 can cause exacerbation of skin MC-mediated allergic inflammation.
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| |
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| Overall design |
Omni-ATAC-seq in unstimulated or stimulated HSMCs, in duplicate, using Illumina NovaSEQ6000 platform.
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| Web link |
https://pubmed.ncbi.nlm.nih.gov/37798647/
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| |
|
| Contributor(s) |
Gao J, Huang H |
| Citation(s) |
37798647 |
| |
| Submission date |
Feb 16, 2022 |
| Last update date |
Oct 07, 2023 |
| Contact name |
HUA HUANG |
| E-mail(s) |
huangh@njhealth.org
|
| Phone |
3033981281
|
| Organization name |
National Jewish Health
|
| Department |
Immunology and Genomic Medicine
|
| Lab |
Huang lab
|
| Street address |
1400 Jackson street, K511
|
| City |
Denver |
| State/province |
Colorado |
| ZIP/Postal code |
80206 |
| Country |
USA |
| |
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| Platforms (1) |
| GPL24676 |
Illumina NovaSeq 6000 (Homo sapiens) |
|
| Samples (6)
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| This SubSeries is part of SuperSeries: |
| GSE196895 |
IL-33 priming and antigenic stimulation synergistically promote the transcription of proinflammatory cytokine and chemokine genes in human skin mast cells |
|
| Relations |
| BioProject |
PRJNA807668 |
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