Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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DNA methylome of human CD4⁺ CLA⁺ T cells in healthy controls and atopic dermatitis patients treated with dupilumab or upadacitinib

ABSTRACT: Skin‑homing CD4⁺CLA⁺ T cells are involved in chronic AD inflammation and may carry long‑lived disease-modifying effects through stable DNA methylation programs. By profiling the DNA methylome of healthy individuals and AD patients before and after one year of dupilumab or upadacitinib. This study tests whether these therapies facilitate epigenetic reprogramming. Using flow cytometry, CD4+CLA+ T cells were isolated from AD patients (n=12) at baseline and after 52 weeks of dupilumab (n=6) or upadacitinib (n=6) treatment. DNA methylome was conducted using the EPIC array. Non-atopic healthy controls (HC) (n=6) were included for comparison.

ORGANISM(S): Homo sapiens

SUBMITTER: Hidde Smits M.

PROVIDER: E-MTAB-16746 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Hereditary Motor and Sensory Neuropathies (HMSN) are the most common inherited peripheral neuropathies and comprise a group of genetically heterogeneous diseases. We study the genetic defects causing three demyelinating disorders: HMSN1A, HMSN-LOM and congenital cateracts facial dysmophism neuropathy (CCFDN) syndrome, which are caused by mutations in PMP22, NDRG1 and CTDP1, respectively. The function and patho-mechanisms of these genes is still unknown. To identify effects downstream of the mutations, thereby possibly involved in the disease process, we used Serial expression of gene expression (SAGE) and microarray analysis. We analyzed human Schwann cell lines from three normal subjects, one HMSN-LOM patient, two HMSN-1A patients and two CCFDN patients and compared our data to a recent dataset of human Schwann cells (4 normal subjects passage 1 vs. 3, GDS1869/GSE4030 M.B. Bunge, 2006). We excluded genes that were not consistently regulated between biological and technical replicates and genes that were found to be influenced by passage number (p<0.05). Comparing expression profiles of demyelinating neuropathies with different mutations we identified: 1. expression signatures specific for each genotype. 2. Genes commonly (dys)regulated in all screened neuropathies. Interestingly, these include genes that play a role in reorganization of sodium channels in central and peripheral nerves (S100A10, CD90), or extracellular matrix remodeling (e.g. TGFBI, SERPINE1, THBS1). We also found high up-regulation of genes involved in Schwann cell lineage and in particular, genes that are associated with an immature or pre-myelinating Schwann cell phenotype (i.e. Sox2, Sox10, COL18A1, TFAP2A, Pax3, CDH19). Our study shows that many genes, possibly contributing to nerve pathology can be identified by this approach. Experiment Overall Design: Experimental design: in total 12 (two-color) arrays were run. All neuropathy samples were in duplicate (technical replicates). Two CCFDN and two HMSN1A patients were also analyzed as biological replicates. Three healthy subjects were included from which one was in duplicate. All samples (Cy3) were compared to a common reference pool (Cy5) which consisted of a mix of all samples.

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DNA methylome of human CD4⁺ CLA⁺ T cells in healthy controls and atopic dermatitis patients treated with dupilumab or upadacitinib

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