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MicroRNA-31 reduces the motility of proinflammatory T helper 1 lymphocytes

ABSTRACT: MicroRNA-31 reduces the motility of proinflammatory T helper 1 lymphocytes

PROVIDER: PRJNA504008 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8165040_1.fastq.gz	Fastqsanger.gz
	SRR8165040_2.fastq.gz	Fastqsanger.gz
	SRR8165041_1.fastq.gz	Fastqsanger.gz
	SRR8165041_2.fastq.gz	Fastqsanger.gz
	SRR8165038_1.fastq.gz	Fastqsanger.gz

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MicroRNA-31 Reduces the Motility of Proinflammatory T Helper 1 Lymphocytes.

Project description:Proinflammatory type 1 T helper (Th1) cells are enriched in inflamed tissues and contribute to the maintenance of chronic inflammation in rheumatic diseases. Here we show that the microRNA- (miR-) 31 is upregulated in murine Th1 cells with a history of repeated reactivation and in memory Th cells isolated from the synovial fluid of patients with rheumatic joint disease. Knock-down of miR-31 resulted in the upregulation of genes associated with cytoskeletal rearrangement and motility and induced the expression of target genes involved in T cell activation, chemokine receptor- and integrin-signaling. Accordingly, inhibition of miR-31 resulted in increased migratory activity of repeatedly activated Th1 cells. The transcription factors T-bet and FOXO1 act as positive and negative regulators of T cell receptor (TCR)-mediated miR-31 expression, respectively. Taken together, our data show that a gene regulatory network involving miR-31, T-bet, and FOXO1 controls the migratory behavior of proinflammatory Th1 cells.

| S-EPMC6291424 | biostudies-literature

MicroRNA-31 reduces the motility of proinflammatory T helper 1 lymphocytes

Project description:We performed total RNA-Seq of murine Th1 cells which were four times reactivated in vitro in the presence of irradiated APC'srepeatedly activated in vitro.

2018-12-19 | GSE122218 | GEO

SARS-COV-2 Uses CD4 to infect T Helper Lymphocytes

Project description:The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2 or CoV-2) is the agent of a major global outbreak of respiratory tract disease known as COVID-19. CoV-2 infects the lungs and may cause several immune-related complications such as lymphocytopenia and cytokine storm which are associated with the severity of the disease and predict mortality. The mechanism by which CoV-2 infection may result in immune system dysfunction is not fully understood. Here we showed that CoV-2 infects human CD4+ T helper cells, but not CD8+ T cells. CoV-2 is found in the blood and bronchoalveolar lavage T helper cells of severe COVID-19 patients. We demonstrated that CoV-2 spike glycoprotein (S) (sCoV-2) directly binds to the CD4 co-receptor, which in turn mediates the entry of CoV-2 in T helper cells in a mechanism that also requires ACE2 and TMPRSS2. Once inside T helper cells, CoV-2 assembles viral factories, impairs cell function and may cause cell death. CoV-2 infected T helper cells express higher amounts of IL-10, which has been associated with viral persistence and disease severity. Thus, CD4-mediated CoV-2 infection of T helper cells may explain the poor adaptive immune response of many COVID-19 patients.

2023-07-28 | PXD020967 | Pride

Deficiency of RPSA reduces binding of P65 to proinflammatory cytokines promoter regions in HSV-1 infection

Project description:After HSV-1 infection, ribosomal protein RPSA can recognize viral DNA and promotes the expression of proinflammatory cytokines. Through ChIP-seq, we found that the enrichment of P65 in proinflammatory cytokines(Il1b, Il6, Il12b, etc.) promoter regions was decreased due to Rpsa deficiency.

2023-11-12 | GSE204891 | GEO

MYBPH, a novel transcriptional target of NKX2-1/TTF-1, inhibits ROCK1 and actomyosin assembly, and reduces cell motility and tumor metastasis

Project description:Cell migration driven by actomyosin filament assembly is a critical step in tumour invasion and metastasis. Herein, we report identification of myosin binding protein H (MYBPH) as a transcriptional target of NKX2-1 (also known as TTF-1 and TITF1), a lineage-survival oncogene in lung adenocarcinoma. MYBPH inhibits assembly competence-conferring phosphorylation of the myosin regulatory light chain (RLC) as well as activating phosphorylation of LIM domain kinase (LIMK). These are unexpectedly implemented through direct physical interaction of MYBPH with Rho kinase 1 (ROCK1) rather than with RLC. In addition, MYBPH is shown to directly bind with non-muscle myosin heavy chain IIA (NMHC IIA), resulting in inhibition of NMHC IIA assembly. Thus, MYBPH plays multi-facetted roles in negative regulation of actomyosin organization, which in turn reduces cell motility, invasion, and metastasis. Finally, we also show that MYBPH is epigenetically inactivated by promoter DNA methylation in a fraction of lung adenocarcinomas abundantly expressing NKX2-1, which appears to be in accordance with its deleterious function for lung adenocarcinoma invasion and metastasis, as well as with the paradoxical association of NKX2-1 expression with favourable prognosis in lung adenocarcinoma patients. Dye-swap experiment, vector control vs. transiently transfectanted with TTF-1 in HPL1D, immortalized human peripheral lung epithelial cell line.

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Characterization of Two Outer Membrane Proteins, FlgO and FlgP, that Influence Vibrio cholerae Motility

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CEBPD suppresses motility-associated gene signatures and reduces pancreatic ductal adenocarcinoma cell migration

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Dendritic cell maturation by proinflammatory TNF or pathogenic Trypanosoma brucei antigens instruct similar T helper-2 cell responses in murine models of autoimmunity and asthma

Project description:Background Dendritic cells (DC) represent the major cell type leading to polarized T helper (Th) cell responses in vivo. The current data indicate that DC maturation under inflammatory conditions or by helminth infections induce only incomplete DC maturation bearing a partially tolerogenic potential. Such semi-mature DC promoted a Th2 profile with increasing proportions of regulatory IL-10 producing T cells (Tr-1) upon restimulation. Methodology/Principal Findings Here we asked whether the instruction of DC by the proinflammatory cytokine TNF is qualitatively different from maturation by two types of variant surface glycoproteins (VSGs) of Trypanosoma brucei. We tested differentially matured murine bone marrow (BM)-derived DC for changes in surface markers or cytokines, by microarray analyses, for their induction of Th2 responses and their capacity to influence the disease models asthma for Th2 immunity and experimental autoimmune encephalomyelitis (EAE) for a Th1/Th17 response. Conclusions/Significance Together, our data suggest that the partial maturation signatures induced by TNF and VSG antigens are highly similar and result in comparable Th2/Tr1 profiles, effects on asthma and EAE. This is remarkable since the responses resulting from endogenous inflammatory TNF-receptor signals or exogenous pathogenic MyD88 ligands are comparable. total samples analysed are 5

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Lipin2 limits macrophage proinflammatory response.

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OGT suppresses macrophage proinflammatory activation

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