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Peptidylarginine deiminases 2 and 4 modulate innate and adaptive immune responses in TLR-7 dependent lupus

ABSTRACT: Peptidylarginine deiminases 2 and 4 modulate innate and adaptive immune responses in TLR-7 dependent lupus

PROVIDER: PRJNA498311 | ENA |

REPOSITORIES: ENA

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Peptidylarginine deiminases 2 and 4 modulate innate and adaptive immune responses in TLR-7 dependent lupus

Project description:Peptidylarginine deiminases (PADs) play critical roles in the development and progression of autoimmune diseases. PAD4 is involved in systemic lupus erythematosus (SLE) pathogenesis while the role of PAD2 in immune dysregulation in SLE is not clear. The differential roles of PAD2 and PAD4 in the progression of murine SLE and in modulation of innate and adaptive immunity were examined. The transcriptome of lymphoid organs from imiquimod-treated PAD2/4 and control mice was characterized and elucidated using RNASeq technology.

2019-01-17 | GSE121751 | GEO

Peptidylarginine deiminases 2 and 4 modulate innate and adaptive immune responses in TLR-7-dependent lupus.

Project description: Not available

| S-EPMC6328098 | biostudies-literature

Peptidylarginine deiminase 4 promotes the renal infiltration of neutrophils and exacerbates the TLR7 agonist-induced lupus mice

Project description:Peptidylarginine deiminase 4 (PAD4), encoded by PADI4, plays critical roles in the immune system. The pathological roles of PAD4 were investigated in lupus model mice. PAD4-regulated pathways were identified by RNA-sequencing of WT and Padi4 KO neutrophils.

2020-02-19 | GSE145422 | GEO

HSV ICP0 recruits USP7 to modulate TLR-mediated innate response.

Project description: Not available

| S-EPMC3401030 | biostudies-literature

Innate vs. adaptive lymphocyte gene expression

Project description:Three innate (B1-B, NKT, CD8aaT cells) and adaptive (B2-B, CD4T, CD8abT cells) cell-types were sorted by FACS. Three biological replicates for NKT, CD4T, CD8aaT, CD8abT cells and two biological replicates for B1 and B2 cells were generated and the expression profiles were determined using Affymetrix Mu74Av2 chip. Comparisons between the sample groups allow the identification of genes differentially expressed between the innate and adaptive cell-types. Keywords: cell type comparison, innate vs. adaptive

2006-01-31 | GSE3039 | GEO

A TLR- and non-TLR-mediated innate response to lentiviruses restricts hepatocyte entry and can be ameliorated by pharmacological blockade

Project description:Lentiviral vector (LV)-mediated gene transfer is a promising method of gene therapy. We previously reported that systemic injection of LV triggers a transient inflammatory response. Here, we carried out studies to better characterize this response, and to develop a strategy to overcome the effects of interferon (IFN) on LV-mediated gene transfer. We profiled gene expression in the liver after LV administration using deep-sequencing, and identified several innate response pathways. We examined the response to LV in MyD88-TRIF knock-out mice, which are incapable of toll-like receptor (TLR) signaling. The IFN response to LV was not reduced in the liver, indicating that a non-TLR pathway can recognize LV in this tissue. Indeed, blocking reverse-transcription with AZT reduced the IFN response only in the liver, suggesting that proviral DNA can be a trigger. To block the inflammatory response, we pre-treated mice with a short-course of dexamethasone. At 4 hours post-treatment, all of the IFN-induced genes were normalized. By blocking the inflammatory response, hepatocyte transduction was dramatically increased, which doubled the level of human factor-IX produced by a hepatocyte-specific LV. Our studies uncover new insights into LV-induced immune responses in the liver, and provide a means to increase the safety and efficiency of LV-mediated gene transfer. mRNA profiles from livers of untreated and LV-treated mice were generated by deep-sequencing in Illumina HiSeq 2000.

2013-07-05 | E-GEOD-39129 | biostudies-arrayexpress

Gene expression in mouse lung homogenates treated with synthetic TLR ligands to induce resistance

Project description:Infectious pneumonias exact an unacceptable mortality burden worldwide. Efforts to protect populations from pneumonia have historically focused on antibiotic development and vaccine-enhanced adaptive immunity. However, we have recently reported that the lungs’ innate defenses can be therapeutically induced by inhalation of a combination of synthetic TLR ligands that synergize to protect mice against otherwise lethal pneumonia. Simultaneous treatment with ligands for TLR2/6 and TLR9 conferred robust, synergistic protection against virulent Gram-positive and Gram-negative pathogens, as well as viruses. Protection is associated with rapid pathogen killing in the lungs, and pathogen killing can be induced from lung epithelial cells in isolation. Here we explore the mechanisms underlying this dramatic phenomenon by performing microarray gene expression analysis of mouse lungs treated by aerosol with PBS (sham treatment), Pam2CSK4 (TLR 2/6 ligand), ODN2395 (TLR9 ligand), or both TLR ligands.

2011-05-01 | GSE28994 | GEO

Innate and Adaptive Immunity in Parkinson Disease

Project description:Innate and Adaptive Immunity in Parkinson Disease

| PRJNA646548 | ENA

Innate and Adaptive Immunity in Parkinson Disease

Project description:Innate and Adaptive Immunity in Parkinson Disease

| PRJNA646549 | ENA

IRF1 governs the differential Interferon-Stimulated Gene responses in human monocytes and macrophages by regulating chromatin accessibility (RNA-seq - TLR stimulation)

Project description:Myeloid lineage cells use TLRs to recognize and respond to diverse microbial ligands. Although unique transcription factors dictate the outcome of specific TLR signaling, whether lineage-specific differences exist to further modulate the quality of TLR-induced inflammation remains unclear. Comprehensive analysis of global gene transcription in human monocytes, monocyte-derived macrophages and monocyte-derived dendritic cells stimulated with various TLR ligands identifies multiple lineage-specific, TLR-responsive gene programs. Monocytes are hyperresponsive to TLR7/8 stimulation that correlates with higher expression of the receptors. While macrophages and monocytes express similar levels of TLR4, macrophages, but not monocytes, upregulate Interferon-Stimulated Genes (ISGs) in response to TLR4 stimulation. We find that TLR4 signaling in macrophages uniquely engages transcription factor IRF1, which facilitates opening of ISG loci for transcription. This study provides a critical mechanistic basis for lineage-specific TLR responses and uncovers IRF1 as a master epigenetic regulator for the ISG transcriptional program in human macrophages.

2021-02-24 | GSE147310 | GEO

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