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E-MTAB-5622

ABSTRACT: Transcriptional profiling of activated CD4+ memory T cells exposed to anti-TNF and recombinant human TNF-alpha in vitro

PROVIDER: E-MTAB-5622 | ExpressionAtlas | 2025-01-23

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-MTAB-5622-analysis-methods.tsv	Tabular
	E-MTAB-5622-analytics.tsv	Tabular
	E-MTAB-5622-atlasExperimentSummary.Rdata	Rdata
	E-MTAB-5622-configuration.xml	Xml
	E-MTAB-5622-g1_g2-mvaPlot.png	Other

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Transcriptional profiling of activated CD4+ memory T cells exposed to anti-TNF and recombinant human TNF-alpha in vitro

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Identification of a transcription factor network that regulates anti-TNF mediated IL-10 expression in human CD4+ T-cells

Project description:CD4+ T-cells are key players in the pathogenesis of rheumatoid arthritis (RA) through potent production of inflammatory mediators including IL-17A, IFNg and TNF. Anti-TNF therapy has revolutionized the treatment of RA and we previously demonstrated that in vitro treatment of human CD4+ T-cells with the anti-TNF monoclonal antibody adalimumab (ADA) promotes anti-inflammatory IL-10 expression in multiple subpopulations of CD4+ T-cells. Here we investigated the transcriptional mechanisms underlying the IL-10 induction by TNF-blockade in in vitro stimulated CD4+ T-cells. CD4+ T-cells were isolated from PBMC of healthy volunteers by magnetic isolation and cultured for 3 days with anti-CD3/CD28 mAb in the absence or presence of anti-TNF. After culture, CD45RA+ cells were depleted and RNA was extracted for gene expression profiling by RNA-seq and cell nuclei were isolated for chromatin accessibility analysis by ATAC-seq. Gene expression analysis of memory CD4+ T-cells showed a distinct gene signature of 183 genes (q-value <0.05) conferred by anti-TNF treatment. Pathway enrichment analysis of the differentially expressed genes revealed multiple pathways related to cytokine signalling and regulation of cytokine production; in particular, IL10 was the most upregulated gene by anti-TNF, while the proinflammatory cytokines and chemokines IFNG, IL9, IL22 and CXCL10 were significantly downregulated (q-value <0.05). Transcription factor (TF) motif analysis at the differentially open chromatin regions after anti-TNF treatment revealed 58 TF motifs, shared by all donors, enriched at the IL10 locus. We identified 7 TF candidates for the anti-TNF mediated regulation of IL-10, which were either differentially expressed or whose locus was differentially accessible upon anti-TNF stimulation. We postulate that this TF network, which includes MAF and PRMD1, drives transcriptional regulation of IL-10 in anti-TNF treated T-cells.

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Transcriptional profiling of activated CD4+ memory T cells exposed to anti-TNF and recombinant human TNF-alpha in vitro

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