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Mapping Genome-wide Accessible Chromatin in Primary Human T Lymphocytes by ATAC-Seq
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Single-cell chromatin accessibility and transcriptomic characterization of Behcet's disease.
Wen Shi1,2, Jinguo Ye1, Zhuoxing Shi1
1State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, 510060, Guangzhou, China.
Communications Biology
|October 17, 2023
Summary
This study reveals the gene activity and epigenetic changes in Behcet's disease (BD) using single-cell multi-omics. It identifies key immune cell regulators involved in inflammation and autoimmunity in BD patients.
Area of Science:
- Immunology
- Genomics
- Epigenetics
Background:
- Behcet's disease (BD) is a chronic vasculitis with complex immune system dysregulation.
- A detailed understanding of gene regulation and immune responses in BD peripheral blood cells is lacking.
Purpose of the Study:
- To comprehensively analyze the gene-regulatory profile and cellular heterogeneity in Behcet's disease.
- To identify cell-type-specific immune responses and potential epigenetic regulators in BD.
Main Methods:
- Multi-omic single-cell analysis of 424,817 cells from BD patients and healthy individuals.
- Simultaneous mapping of chromatin accessibility and gene expression.
- Integrative analysis to predict transcription factor (TF) regulators and gene-regulatory networks.
Main Results:
- Identified widespread cell-type-specific, disease-associated active and pro-inflammatory immune responses.
- Uncovered the epigenetic and transcriptional landscape in BD peripheral blood.
- Predicted key TF regulators, including AP-1, NF-kB, and ETS families, involved in BD pathogenesis.
Conclusions:
- The study provides a detailed multi-omic map of BD peripheral blood, highlighting epigenetic and transcriptional alterations.
- Identified potential regulatory networks governing inflammation and cellular interactions in Behcet's disease.
- Expands understanding of the immunopathology of BD at the epigenomic level.

