C1q reprograms innate immune memory [ChIP-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1130479 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR29666676_1.fastq.gz | Fastqsanger.gz | |||
| SRR29666676_2.fastq.gz | Fastqsanger.gz | |||
| SRR29666677_1.fastq.gz | Fastqsanger.gz | |||
| SRR29666677_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 7 |
Similar Datasets
Project description:C1q reprograms innate immune memory [RNA-seq]
| PRJNA1130475 | ENA
Project description:Innate immune memory, also called trained immunity, is a metabolic and epigenetically regulated process that enables innate immune cells to recalibrate their inflammatory reactivity in response to pathogenic or endogenous stimuli. In addition to its function in host defense, trained immunity contributes to diverse immune-mediated diseases. We discovered that complement component 1q (C1q) is an effective modulator of innate immune memory, potently suppressing the responsiveness of myeloid cells. We found that C1q leads to profound reprogramming of myeloid cell metabolism, particularly glycolysis, and exerts control over the transcriptional regulation of important metabolic and inflammatory genes. We corroborate our findings by identifying single-nucleotide polymorphisms close to the C1q gene that are linked to induction of trained immunity in healthy volunteers. Our results reveal a novel immunomodulatory role for C1q and provide evidence of a molecular interaction between the complement system and innate immune memory. These findings expand our understanding of innate immune memory and provide a promising new target for therapeutic intervention.
2025-06-16 | GSE271219 | GEO
Project description:Innate immune memory, also called trained immunity, is a metabolic and epigenetically regulated process that enables innate immune cells to recalibrate their inflammatory reactivity in response to pathogenic or endogenous stimuli. In addition to its function in host defense, trained immunity contributes to diverse immune-mediated diseases. We discovered that complement component 1q (C1q) is an effective modulator of innate immune memory, potently suppressing the responsiveness of myeloid cells. We found that C1q leads to profound reprogramming of myeloid cell metabolism, particularly glycolysis, and exerts control over the transcriptional regulation of important metabolic and inflammatory genes. We corroborate our findings by identifying single-nucleotide polymorphisms close to the C1q gene that are linked to induction of trained immunity in healthy volunteers. Our results reveal a novel immunomodulatory role for C1q and provide evidence of a molecular interaction between the complement system and innate immune memory. These findings expand our understanding of innate immune memory and provide a promising new target for therapeutic intervention.
2025-06-16 | GSE271218 | GEO
Project description:PAMPS and Innate Immune Memory
| PRJNA1004311 | ENA
Project description:Acid ceramidase regulates innate immune memory
| PRJNA779737 | ENA
Project description:Epigenetic regulation of innate immune memory in microglia
| PRJNA732928 | ENA
Project description:Innate memory is a key defence mechanism against infection, enhancing protective immunity and limiting unnecessary collateral tissue damage. Inflammation triggered by endogenous stimuli that signal cellular stress or tissue injury, must also be tightly controlled to balance robust response to intrinsic danger whilst avoiding catastrophic autoimmunity. Here, we assess the contribution of innate memory to this balance. The extracellular matrix protein tenascin-C, a damage-associated, toll-like receptor 4 (TLR4) agonist, reprograms monocyte response to subsequent threat, inducing concomitantly suppressed and enhanced responses to rechallenge. Comparative analysis of memory evoked by tenascin-C and the pathogenic TLR4 agonist, LPS, revealed both common and distinct gene expression signatures, effects that were controlled transcriptionally, These data highlight how intrinsic and extrinsic innate re-programming exerts control over dysregulated inflammatory networks driving either infectious or chronic ‘sterile’ inflammatory diseases.
2025-05-06 | GSE273837 | GEO
Project description:Gene Expression Regulation in Brain Underlying Innate Immune Memory
| PRJNA693876 | ENA
Project description:Exposure to pathogen-associated molecular patterns (PAMPs) induces an augmented, broad-spectrum antimicrobial response to subsequent infection, a phenomenon termed innate immune memory. This study examined the effects of treatment with β-glucan, a fungus-derived Dectin-1 ligand, and monophosphoryl lipid A (MPLA), a bacteria-derived TNS4 ligand, on innate immune memory with a focus on identifying common cellular and molecular pathways. Treatment with either PAMP prepared the innate immune system to respond more robustly to Pseudomonas aeruginosa infection in vivo by facilitating mobilization of innate leukocytes into blood, their recruitment to the site of infection, augmentation of microbial clearance and attenuation of cytokine production. Examination of macrophages ex vivo showed that metabolism, phagocytosis and respiratory burst were amplified by treatment with either agent, although MPLA more robustly augmented these activities and more effectively facilitated killing of bacteria. Both agents activated gene expression pathways in macrophages that control inflammation, antimicrobial functions and protein synthesis and suppressed pathways regulating cell division with MPLA more potently inducing global gene transcription. β-glucan treatment minimally modified macrophage differential gene expression in response to LPS challenge compared to control whereas MPLA attenuated the magnitude of the LPS-induced transcriptional response. These results show that b-glucan and MPLA similarly augment the innate response to infection in vivo. Yet, MPLA more potently induces alterations in macrophage metabolism, antimicrobial functions, gene transcription and the response to LPS.
2023-08-23 | GSE240614 | GEO
Project description:Galectin-7 reprograms skin carcinogenesis by fostering innate immune evasive programs
| PRJNA693872 | ENA