Ontology highlight
ABSTRACT:
PROVIDER: PRJNA513292 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8403840_1.fastq.gz | Fastqsanger.gz | |||
| SRR8403840_2.fastq.gz | Fastqsanger.gz | |||
| SRR8403850_1.fastq.gz | Fastqsanger.gz | |||
| SRR8403850_2.fastq.gz | Fastqsanger.gz | |||
| SRR8403860_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 168 |
Similar Datasets
Project description:Innate immune responses of plant cells confer the first line of defence against pathogens. Signals generated by activated receptors are integrated inside the cell and converge on transcriptional programmes in the nucleus. The Arabidopsis Toll-related intracellular receptor RPS4 operates inside nuclei to trigger resistance and defence gene reprogramming through the stress response regulator, EDS1. Using RNA-seq, we analyzed the early RPS4-mediated transcriptional changes over time in a temperature-conditioned and pathogen-independent system.
2017-12-11 | GSE80448 | GEO
Project description:Innate immune responses of plant cells confer the first line of defence against pathogens. Signals generated by activated receptors are integrated inside the cell and converge on transcriptional programmes in the nucleus. The Arabidopsis Toll-related intracellular receptor RPS4 operates inside nuclei to trigger resistance and defence gene reprogramming through the stress response regulator, EDS1. Using RNA-seq, we analyzed the early RPS4-mediated transcriptional changes over time in a temperature-conditioned and pathogen-independent system.
2017-12-11 | GSE80424 | GEO
Project description:Increased researches show that complement, the codominant central mediator of humoral immunity, is a critical factor in tumor initiation, development, and chemotherapy resistance. C5a/C5aR1 signaling has been shown to promote tumor progression by recruiting MDSCs in breast malignancies And blockade of C5aR1 resets M1 via gut microbiota-mediated PFKM stabilization in a TLR5-dependent manner. We here report that TLR5 as a key regulator of tumor associated macrophages M1 polarization. Flagellin, the protein subunit of the bacterial flagellum, stimulates the innate immune receptor Toll-like receptor 5 (TLR5) after pattern recognition. Receptor activity was turned by a TLR5-flagellin interaction distal to the site of pattern recognition. Thus, activation of downstream signaling pathway is promoted.
2024-01-20 | GSE252048 | GEO
Project description:B-lymphocytes play major adaptive immune roles, producing antibody and driving cell mediated responses. However, how B-cells acutely differentiate in response to receptor signaling codes, including T-cell dependent versus independent cues, remains incompletely understood. To gain insights, we used multi-omic profiling to characterize ex vivo primary human B-cell transcriptomic, proteomic and metabolomic remodeling by B-cell receptor (BCR), Toll-like receptor 9 (TLR9), CD40-ligand (CD40L), interleukin-4 (IL4) or combinations thereof, highlighting key stimulus-specific phenotypes.
2024-06-26 | GSE232769 | GEO
Project description:Toll mediates a robust and effective innate immune response across vertebrates and invertebrates. In Drosophila melanogaster, activation of Toll by systemic infection drives the accumulation of a rich repertoire of immune effectors in hemolymph, including the recently characterized Bomanins as well as the classical antimicrobial peptides (AMPs). Here we report the functional characterization of a Toll-induced hemolymph protein encoded by the bombardier (CG18067) gene. Using the CRISPR-Cas9 system to generate a precise deletion, we found that Bombardier is required for Toll-mediated defense against fungi and Gram-positive bacteria. Assaying cell-free hemolymph from these flies, we found that the Bomanin-dependent candidacidal activity observed in hemolymph is also dependent on Bombardier, but not on the antifungal AMPs Drosomycin and Metchnikowin. Using mass spectrometry, we demonstrated that deletion of Bombardier results in the specific absence of short-form Bomanins from hemolymph. Flies lacking Bombardier also exhibited a defect in pathogen tolerance that we trace to an autoimmune disorder triggered by Toll activation. These results lead us to a model in which the presence of Bombardier in wild-type flies enables the proper folding, secretion, or intermolecular associations of short-form Bomanins, and the absence of Bombardier disrupts one or more of these steps, resulting in defects in both immune resistance and tolerance.
2019-10-25 | MSV000084509 | MassIVE
Project description:The innate immune system is a two-edged sword; it is absolutely required for host defense against infection, but if left uncontrolled can trigger a plethora of inflammatory diseases. Here we used systems biology approaches to predict and validate a gene regulatory network involving a dynamic interplay between the transcription factors NF-κB, C/EBPδ, and ATF3 that controls inflammatory responses. We mathematically modeled transcriptional regulation of Il6 and Cebpd genes and experimentally validated the prediction that the combination of an initiator (NF-κB), an amplifier (C/EBPδ) and an attenuator (ATF3) forms a regulatory circuit that discriminates between transient and persistent Toll-like receptor 4-induced signals. Our results suggest a mechanism that enables the innate immune system to detect the duration of infection and to respond appropriately. Experiment Overall Design: Bone marrow-derived macrophages stimulated with LPS for 0, 20, 40, 60, 80, 120, 240 and 360 minutes.
2009-04-04 | E-GEOD-14769 | biostudies-arrayexpress
Project description:Brucellosis is a critical zoonotic disease impacting humans and animals globally, causing symptoms like fever and arthritis in humans and reproductive issues in animals. The disease stems from the Brucella genus, adept at evading the immune system and proliferating within host cells. This study explores how Brucella abortus manipulates host cellular mechanisms to sustain infection, focusing on the interaction with murine macrophages over 24 hours. Initial host defenses involve innate immune responses, while Brucella's survival strategies include evading lysosomal degradation and modulating host cell functions through various pathways. The research identified significant transcriptional changes in macrophages post-infection, highlighting pathways such as cytokine storm, pyroptosis signaling, Toll-like receptor pathways and LXRs/RXRs signaling. The findings shed light on Brucella's complex mechanisms to undermine host defenses and underscore the need for further investigation into therapeutic targets to combat brucellosis.
2024-09-30 | E-MTAB-13990 | biostudies-arrayexpress
Project description:A dysbiosis in the intestinal microbiome plays a role in the pathogenesis of several immunological diseases. These diseases often show a gender bias, suggesting gender differences in immune responses and in the intestinal microbiome. We hypothesized that gender differences in immune responses are associated with gender differences in microbiota. We demonstrated mouse strain dependent gender differences in the intestinal microbiome. Interestingly, a cluster of colonic genes (related to humoral and cell-mediated immune responses) correlated oppositely with microbiota species abundant in B6 females and in BALB/c males. This suggests that with different genetic backgrounds, gender associated immune responses are differentially regulated by microbiota. The net result was the same, since both mouse strains showed similar gender induced differences in immune cell populations in the mesenteric lymph nodes. Therefore, host-microbe interactions might be more complicated than assumed, as bacterial-species adaptations might be highly dependent on the genetic make-up of the individual.
2018-06-27 | GSE85911 | GEO
Project description:A dysbiosis in the intestinal microbiome plays a role in the pathogenesis of several immunological diseases. These diseases often show a gender bias, suggesting gender differences in immune responses and in the intestinal microbiome. We hypothesized that gender differences in immune responses are associated with gender differences in microbiota. We demonstrated mouse strain dependent gender differences in the intestinal microbiome. Interestingly, a cluster of colonic genes (related to humoral and cell-mediated immune responses) correlated oppositely with microbiota species abundant in B6 females and in BALB/c males. This suggests that with different genetic backgrounds, gender associated immune responses are differentially regulated by microbiota. The net result was the same, since both mouse strains showed similar gender induced differences in immune cell populations in the mesenteric lymph nodes. Therefore, host-microbe interactions might be more complicated than assumed, as bacterial-species adaptations might be highly dependent on the genetic make-up of the individual.
2018-06-27 | GSE85912 | GEO
Project description:DC-SIGN is a C-type lectin expressed by dendritic cells (DCs) that binds HIV-1, sequestering it within multivesicular bodies to facilitate transmission to CD4+ T cells. Here we characterize the molecular basis of signalling through DC-SIGN by large-scale gene expression profiling and phosphoproteome analysis. Solitary DC-SIGN activation leads to a phenotypically disparate transcriptional program from Toll-like receptor (TLR) triggering with downregulation of MHC II, CD86, and interferon response genes and with induction of the TLR negative regulator ATF3. Phosphoproteome analysis reveals DC-SIGN signals through the leukemia-associated Rho guanine nucleotide exchange factor (LARG) to induce Rho activity. This LARG activation also occurs on DC HIV exposure and is required for effective HIV viral synapse formation. Taken together HIV mediated DC-SIGN signalling provides a mechanism by which HIV evades the immune response yet induces viral spread. Keywords: Activation state, signalling, Toll-like Receptor (TLR)
2007-04-24 | GSE6090 | GEO