RNA-sequencing analysis of the effect of progesterone on T cell activation
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA680365 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13120900_1.fastq.gz | Fastqsanger.gz | |||
| SRR13120900_2.fastq.gz | Fastqsanger.gz | |||
| SRR13120901_1.fastq.gz | Fastqsanger.gz | |||
| SRR13120901_2.fastq.gz | Fastqsanger.gz | |||
| SRR13120902_1.fastq.gz | Fastqsanger.gz |
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Project description:The changes in progesterone (P4) levels during and after pregnancy coincide with the temporary improvement and worsening of several autoimmune diseases like multiple sclerosis (MS) and rheumatoid arthritis (RA). Most likely immune-endocrine interactions play a major role in these pregnancy-induced effects. In this study, we used next generation sequencing to investigate the direct effects of P4 on CD4+ T cell activation, of central importance in pregnancy and disease. We found that P4 had a profound dampening effect on T cell activation, altering the gene and protein expression profile and reversing many of the changes induced during the activation. The transcriptomic changes induced by P4 were significantly enriched for genes associated with diseases known to be modulated during pregnancy such as MS, RA and psoriasis. The TH1-and TH17-associated transcription factors STAT1 and STAT3 were significantly downregulated by P4 and their downstream targets were significantly enriched among the diseases-associated genes. Several of these genes included well-known and disease-relevant cytokines, such as IL-12β, CXCL10 and OSM, that were further validated also at the protein level using proximity extension assay. Our results extend the previous knowledge of P4 as an immune regulatory hormone and support its importance during pregnancy for regulating potentially detrimental immune responses towards the semi-allogenic fetus. Further, our results also point toward a potential role for P4 in the pregnancy-induced disease immunomodulation, suggestively through dampening of TH1 and TH17-associated immune responses and highlight the need for further studies evaluating P4 as a future treatment option.
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Project description:T-helper 1 responses are involved in the development of many autoimmune diseases such as Multiple sclerosis (MS). MS is a relapse remitting disease that eventually progresses to a progressive neurodegenerative disease. During pregnancy the relapse rate of MS is significantly reduced with peak reduction during the third trimester followed by an increase in relapse rate post-partum. One of the highest expressed hormones during pregnancy is progesterone. Progesterone has been show to have an inhibiting effect on T-cell activation and been proposed to promote a T-regulatory like cell state. To evaluate the influence of progesterone on the chromatin and gene expressive state of T-helper type 1 cells we differentiated primary human naïve T-cell in the presence progesterone with sampling at 0.5, 1, 2, 6 and 24 hours and performed ATAC-seq and RNA-seq.
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Project description:Steroid hormones are well-recognized suppressors of the inflammatory response, however, their cell- and tissue-specific effects in the regulation of inflammation are far less understood, particularly for the sex-related steroids. To determine the contribution of progesterone in the endothelium, we have characterized and validated an in vitro culture system in which human umbilical vein endothelial cells constitutively express human progesterone receptor (PR). Using next generation RNA-sequencing, we identified a selective group of cytokines that are suppressed by progesterone both under physiological conditions and during pathological activation by lipopolysaccharide. In particular, IL-6, IL-8, CXCL2/3, and CXCL1 were found to be direct targets of PR, as determined by ChIP-sequencing. Regulation of these cytokines by progesterone was also confirmed by bead-based multiplex cytokine assays and quantitative PCR. These findings provide a novel role for PR in the direct regulation of cytokine levels secreted by the endothelium. They also suggest that progesterone-PR signaling in the endothelium directly impacts leukocyte trafficking in PR-expressing tissues Examination of PR target genes in human umbilical vein endothelial cells (HUVECs) using RNA-seq PR infected only (PR); PR infected followed by ligand treatment (PR+P); PR infected followed by 4h LPS treatment (PR+LPs_4h); PR infected followed by 8h LPS treatment (PR+LPs_8h); PR infected followed by 4h LPS and progesterone treatment (PR+LPS+P_4h); PR infected followed by 8h LPS and progesterone treatment (PR+LPS+P_8h)
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