NCBI Logo
GEO Logo
   NCBI > GEO > Accession DisplayHelp Not logged in | LoginHelp
GEO help: Mouse over screen elements for information.
          Go
Series GSE184237 Query DataSets for GSE184237
Status Public on Apr 26, 2022
Title Epigenetic and Transcriptional Dysregulation in T cells of patients with Atopic Dermatitis [RNA-Seq]
Organism Homo sapiens
Experiment type Expression profiling by high throughput sequencing
Summary Atopic dermatitis (AD), the start of the atopic march, is one of the most common skin disorders in children. Immunologically, AD involves skin barrier defects and CD4+ T cells that localize to the skin, producing inflammatory cytokines and amplifying epidermal dysfunction. To understand the gene regulatory activity differences in peripheral blood T cells in AD, we measured chromatin accessibility (ATAC-seq), NFKB1 binding (ChIP-seq), and gene expression (RNA-seq) in stimulated CD4+ T cells from subjects with active moderate-to-severe AD and age-matched healthy, non-allergic controls. Chromatin accessibility in stimulated CD4+ T cells were highly enriched for AD genetic risk variants. The vast majority of ATAC-seq peaks were shared, consistent with those sections of chromatin being equally available between matched pairs; however, NFKB DNA binding motifs were enriched in chromatin accessible in an AD-dependent manner. NFKB1 ChIP-seq identified peaks that were stronger in AD cases, enriched in controls, or shared between cases and controls. The ChIP-seq peaks that were statistically stronger in AD were more strongly enriched for NFKB DNA binding motifs. Chromatin that was more strongly accessibe and bound by NFKB1 in AD were enriched for genetic variants that increase risk for AD. Using whole genome sequencing data, we identified wide-spread genotype-dependent chromatin accessibility and allelic NFKB1 binding at AD and allergic disease genetic risk loci.
 
Overall design RNA-seq was performed in stimulated CD4+ T cells from 6 subjects with active moderate-to-severe AD and 6 age-matched healthy, non-allergic controls.
 
Contributor(s) Kottyan LC, Weirauch MT
Citation(s) 35576187
NIH grant(s)
Grant ID Grant title Affiliation Name
R01 HG010730 Virus-driven human gene misregulation in disease CHILDREN'S HOSPITAL MEDICAL CENTER Matthew Tyson Weirauch
R01 NS099068 Binding of Epstein Barr Virus EBNA2 unifies multiple sclerosis genetic mechanisms CHILDREN'S HOSPITAL MEDICAL CENTER Matthew Tyson Weirauch
R01 GM055479 Biochemical and Computational Analysis of Notch signal transduction CHILDREN'S HOSPITAL MEDICAL CENTER Matthew Tyson Weirauch
U01 AI130830 Gene Regulation as a Foundation for Autoimmune Disease Prevention CHILDREN'S HOSPITAL MEDICAL CENTER Matthew Tyson Weirauch
R01 DK107502 Mechanisms of genetic risk at 2p23 in Eosinophilic Esophagitis CHILDREN'S HOSPITAL MEDICAL CENTER Leah Claire Kottyan
R01 AI148276 Genomics of Inflammatory Bowel Disease CHILDREN'S HOSPITAL MEDICAL CENTER Leah Claire Kottyan
U19 AI070235 Epithelial Genes in Allergic Inflammation CHILDREN'S HOSPITAL MEDICAL CENTER Gurjit K. Khurana Hershey
U01 HG011172 Polygenic Risk Scores for Healthier African American Families CHILDREN'S HOSPITAL MEDICAL CENTER Leah Claire Kottyan
P30 AR070549 Cincinnati Rheumatic Diseases Resource Center CHILDREN'S HOSPITAL MEDICAL CENTER SUSAN D THOMPSON
R01 AR073228 Transcription Factor Genetics in Lupus CHILDREN'S HOSPITAL MEDICAL CENTER Leah Claire Kottyan
R01 AR073228 Transcription Factor Genetics in Lupus CHILDREN'S HOSPITAL MEDICAL CENTER Matthew Tyson Weirauch
R01 AI024717 Genetic Linkage in Lupus CHILDREN'S HOSPITAL MEDICAL CENTER Leah Claire Kottyan
R01 AI024717 Genetic Linkage in Lupus CHILDREN'S HOSPITAL MEDICAL CENTER Matthew Tyson Weirauch
Submission date Sep 15, 2021
Last update date Oct 23, 2023
Contact name Matthew Weirauch
E-mail(s) Matthew.Weirauch@cchmc.org
Organization name Cincinnati Children's Hospital Medical Center
Department Center for Autoimmune Genomics and Etiology (CAGE)
Street address 3333 Burnet Avenue
City Cincinnati
State/province Ohio
ZIP/Postal code 45229-3026
Country USA
 
Platforms (1)
GPL23227 BGISEQ-500 (Homo sapiens)
Samples (12)
GSM5582243 RNA-seq: Atopic Dermatitis subject 1 (AD1)
GSM5582244 RNA-seq: Atopic Dermatitis subject 2 (AD2)
GSM5582245 RNA-seq: Atopic Dermatitis subject 3 (AD3)
This SubSeries is part of SuperSeries:
GSE184238 Epigenetic and Transcriptional Dysregulation in T cells of patients with Atopic Dermatitis
Relations
BioProject PRJNA763648
SRA SRP337279

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE184237_RAW.tar 1.3 Gb (http)(custom) TAR (of BW, TSV)
SRA Run SelectorHelp
Raw data are available in SRA
Processed data provided as supplementary file

| NLM | NIH | GEO Help | Disclaimer | Accessibility |
NCBI Home NCBI Search NCBI SiteMap