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Regulatory T cells and IFN-γ-producing Th1 cells play a critical role in the pathogenesis of Sjögren’s Syndrome

ABSTRACT: Regulatory T cells and IFN-γ-producing Th1 cells play a critical role in the pathogenesis of Sjögren’s Syndrome

PROVIDER: PRJNA1064171 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27532319_1.fastq.gz	Fastqsanger.gz
	SRR27532319_2.fastq.gz	Fastqsanger.gz
	SRR27532320_1.fastq.gz	Fastqsanger.gz
	SRR27532320_2.fastq.gz	Fastqsanger.gz
	SRR27532321_1.fastq.gz	Fastqsanger.gz

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Regulatory T cells and IFN-γ-producing Th1 cells play a critical role in the pathogenesis of Sjögren’s Syndrome

Project description:Regulatory T cells and IFN-γ-producing Th1 cells play a critical role in the pathogenesis of Sjögren’s Syndrome

| PRJNA1066294 | ENA

Regulatory T cells and IFN-γ-producing Th1 cells play a critical role in the pathogenesis of Sjögren’s Syndrome

Project description:Sjogren’s Disease (SjD) is an autoimmune disorder characterized by progressive inflammation and destruction of both salivary and lacrimal gland leading to dysfunction, as well as extra glandular manifestations. The etiology and pathophysiology of SjD are incompletely understood. Regulatory T (Treg) cells are critical for immunological tolerance. Although Treg abnormalities have been implicated in the pathogenesis of several autoimmune diseases, their role in SjD remains ambiguous. We had previously shown that the function and development of Treg cells depend on store-operated Ca2+ entry (SOCE), which is mediated by ORAI1 Ca2+ channels and stromal interaction molecules (STIM) 1 and 2 following T cell receptor (TCR) stimulation. The ablation of SOCE in Treg cells causes SjD-like disease with increased Th1 and interferon gene expression signatures in the inflamed salivary glands of mice. Here we show enhanced Th1 gene expression signatures and type I and II interferon responses in the peripheral blood mononuclear cells (PBMCs) of human patients with SjD compared to non-SjD controls. We also identified attenuated gene expression in memory Treg cells of patients with SjD. These data from mice and human patients provide new evidence for a critical role of Treg cells and IFNγ producing Th1 cells in the pathogenesis of SjD.

2024-11-04 | GSE253568 | GEO

Regulatory T cells and IFN-γ-producing Th1 cells play a critical role in the pathogenesis of Sjögren’s Syndrome

Project description:Sjogren’s Disease (SjD) is an autoimmune disorder characterized by progressive salivary and lacrimal gland dysfunction, inflammation, and destruction, and extra glandular manifestations. The etiology and pathophysiology of SjD are incompletely understood. Regulatory T (Treg) cells are critical for immunological tolerance and although Treg abnormalities have been implicated in the pathogenesis of several autoimmune diseases, their role in SjD remains ambiguous. We here show that Stim1fl/flStim2fl/flFoxp3-Cre (Stim1/Stim2 Foxp3cre) mice develop a SjD-like phenotype, including severe sialadenitis with hyposalivation, lacrimal gland (LG) inflammation with dry eye and corneal damage, increased anti-Ro and anti-La autoantibody levels and interstitial lung disease. At the cellular level, salivary gland inflammation in Stim1/2Foxp3 mice is characterized by infiltration with CD4+ and CD8+ T cells, which is dominated by a T helper (Th) 1 and Th2 immune response. The changes in gene expression in SGs of mice correlate strongly with transcriptional and epigenetic dysregulation found in SjD patients. Our findings in Stim1/Stim2 Foxp3cre mice provide new evidence for a critical role of Treg cells and IFNγ producing Th1 cells in mediating SjD progression.

2024-11-04 | GSE253188 | GEO

Purified CD123+BDCA4+ plasmacytoid dendritic sorted cell-population derived from IFN signature positive primary Sjögren’s syndrome patients and IFN signature negative primary Sjögren’s syndrome patients compared to Healthy Control individuals

Project description:The IFN type I signature is present in over half of primary Sjögren’s syndrome (pSS) patients and associated with higher disease-activity and autoantibody presence. Plasmacytoid dendritic cells (pDCs) are considered to be the source of enhanced IFN type I expression. The objective of this study was to unravel the molecular pathways underlying IFN type I bioactivity in pDCs of pSS patients. We used microarray gene expression analysis to detail the programme of gene expression underlying IFN type I bioactivity in pDCs of primary Sjogrens' Syndrome patients.

2016-09-28 | GSE83558 | GEO

IFN-g producing Th1 cells induce different transcriptional profiles in microglia and astrocytes

Project description:Autoreactive T cells that infiltrate into the central nervous system (CNS) are believed to have a significant role in mediating the pathology of neurodegenerative diseases such as Alzheimer's disease, amyotrophic lateral sclerosis and multiple sclerosis. Their interaction with microglia and astrocytes in the CNS is crucial for the regulation of the neuroinflammatory process. Our previous work demonstrated that effectors secreted by Th1 and Th17 cells have different capacities to influence the phenotype and function of the glial cells. We have shown that Th1 effectors altered the phenotype and function of both microglia and astrocytes whereas Th17 effectors induced direct effects only on astrocytes but not on microglia. Here we investigated if effector molecules associated with IFN-g producing Th1 cells induced different gene expression profiles in microglia and astrocytes. We performed a microarray analysis of RNA isolated from microglia and astrocytes treated with medium and Th1 culture supernatants and compared the gene expression data. By using the criteria of 2-fold change and a false discovery rate of 0.01 (corrected p-value < 0.01), we demonstrated that a total of 2106 and 1594 genes were differentially regulated microglia and astrocytes respectively in response to Th1-derived factors. We observed that Th1 associated effectors induce distinct transcriptional changes in microglia and astrocytes in addition to commonly regulated transcripts. These distinct transcriptional changes regulate distinct physiological functions and this knowledge can help in better understanding of T cell mediated neuropathologies.

2018-12-03 | GSE113579 | GEO

IFN-g producing Th1 cells induce different transcriptional profiles in microglia and astrocytes

Project description:IFN-g producing Th1 cells induce different transcriptional profiles in microglia and astrocytes

| PRJNA453143 | ENA

The transcription factor Bhlhe40 is a switch of inflammatory versus anti-inflammatory Th1 cell fate determination

Project description:Type 1 T helper (Th1) cells play a critical role in host defense against intracellular pathogens and in autoimmune diseases by producing a key inflammatory cytokine interferon (IFN)-γ; some Th1 cells can also be anti-inflammatory through producing IL-10. However, the molecular switch for regulating the differentiation of inflammatory and anti-inflammatory Th1 cells is still elusive. Here we show that Bhlhe40-deficient CD4 Th1 cells produced less IFN-γ but substantially more IL-10 than wild type Th1 cells. Bhlhe40-mediated IFN-γ production was independent of transcription factor T-bet regulation. Mice with conditional deletion of Bhlhe40 in T cells succumbed to Toxoplasma gondii infection and blockage of IL-10 signaling during infection rescued these mice from death. Thus, our results demonstrate that transcription factor Bhlhe40 is a molecular switch for determining the fate of inflammatory and anti-inflammatory Th1 cells.

2018-05-10 | GSE103173 | GEO

Identification of M3 muscarinic acetylcholine receptor reactive Th17 cells in patients with primary Sjögren’s syndrome

Project description:Previously M3 muscarinic acetylcholine receptore (M3R) reactive Th1 cells were identified, and here, M3R reactive Th17 cells were identified in peripheral blood of primary Sjögren’s syndrome patients using ELISpot method. To assess TCR repertoire overlap between identified M3R reactive Th17 cells, and salivary gland infiltrating T cells, we performed high throughput TCR sequencing of those cells from pSS patient.

2021-04-18 | GSE148966 | GEO

Farnesylation in Th1 cells assessed by click chemistry

Project description:T helper cell activation is highly regulated to ensure proper immune responses while avoiding autoimmune reactions. Cell functions are determined by regulation of various levels of gene expression including posttranslational modifications of proteins. Protein prenylation is a posttranslational modification, where either a farnesyl- or a geranylgeranyl residue is added to a protein. It was shown to play a role in the differentiation and activation of various T cell populations, including Th1 cells. However, it is largely unknown which proteins are prenylated in Th1 cells and what the effect of farnesyl transferase inhibitor treatment, which blocks farnesylation of proteins, on protein prenylation is in this context. Here, using mass spectrometry, we show the identification of farnesylated proteins in human Th1 cells. This approach additionally uncovered the farnesylation of proteins, not yet known to be prenylated. These data provide valuable insights into novel aspects of protein prenylation in Th1 cell activation and deepen our understanding of the effects of farnesyl transferase inhibitor treatment on the human immune system.

2025-01-18 | MSV000096890 | MassIVE

Prenylation in Th1 cells assessed by click chemistry

Project description:T helper cell activation is highly regulated to ensure proper immune responses while avoiding autoimmune reactions. Cell functions are determined by regulation of various levels of gene expression including posttranslational modifications of proteins. Protein prenylation is a posttranslational modification, which can be influenced by statin treatment and was shown to play a role in the differentiation and activation of various T cell populations, including Th1 cells. However, it is largely unknown which proteins are prenylated in Th1 cells and what the effect of statin treatment on protein prenylation is in this context. Here, using mass spectrometry, we show the comprehensive identification of prenylated proteins in human Th1 cells including changes during their activation, before analyzing the effect of statin treatment on this process. This approach additionally uncovered the prenylation of proteins, not yet known to be prenylated, including so far unknown motifs. These data provide valuable insights into novel aspects of protein prenylation in Th1 cell activation and deepen our understanding of the intended or unintended effects of statin treatment on the human immune system.

2024-08-12 | MSV000095575 | MassIVE

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