Metastasis-entrained eosinophils enhance lymphocyte-1 mediated anti-tumor immunity
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA752166 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15347146.fastq.gz | Fastqsanger.gz | |||
| SRR15347147.fastq.gz | Fastqsanger.gz | |||
| SRR15347148.fastq.gz | Fastqsanger.gz | |||
| SRR15347149.fastq.gz | Fastqsanger.gz | |||
| SRR15347150.fastq.gz | Fastqsanger.gz |
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Project description:The recognition of the immune system as a key component of the tumor microenvironment (TME) led to promising therapeutics. Since such therapies benefit only subsets of patients, understanding the activities of immune cells in the TME is required. Eosinophils are an integral part of the TME especially in mucosal tumors. Nonetheless, their role in the TME and the environmental cues that direct their activities are largely unknown, especially in metastasis. We report that breast cancer-driven lung metastasis is characterized by resident and recruited eosinophils. Eosinophil recruitment to the metastatic lung was regulated by G protein coupled receptor signaling but independent of CCR3. Functionally, eosinophils promoted lymphocyte-mediated anti tumor immunity. Transcriptome and proteomic analyses identified the TME rather than intrinsic differences between eosinophil subsets as a key instructing factor directing anti tumorigenic eosinophil activities. Specifically, TNF-a/IFN-g-activated eosinophils facilitated CD4+ and CD8+ T cell infiltration and promoted anti-tumor immunity. Collectively, we identify a mechanism by which the TME entrains eosinophils to adopt anti-tumorigenic properties, which may lead to the development of eosinophil-targeted therapeutics.
2021-07-27 | PXD027596 | Pride
Project description:The recognition of the immune system as a key component of the tumor microenvironment (TME) led to promising therapeutics. Since such therapies benefit only subsets of patients, understanding the activities of immune cells in the TME is required. Eosinophils are an integral part of the TME especially in mucosal tumors.Nonetheless, their role in the TME and the environmental cues that direct their activities are largely unknown, especially in metastasis. We report that breast cancer-driven lung metastasis is characterized by resident and recruited eosinophils. Eosinophil recruitment to the metastatic lung was regulated by G protein coupled receptor signaling but independent of CCR3. Functionally, eosinophils promoted lymphocyte-mediated anti53 tumor immunity. Transcriptome and proteomic analyses identified the TME rather than intrinsic differences between eosinophil subsets as a key instructing factor directing anti tumorigenic eosinophil activities. Specifically, TNF-a/IFN-g-activated eosinophils facilitated CD4+ and CD8+ T cell infiltration and promoted anti-tumor immunity. Collectively, we identify a mechanism by which the TME entrains eosinophils to adopt anti-tumorigenic properties, which may lead to the development of eosinophil-targeted therapeutics.
2021-08-06 | GSE181491 | GEO
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Project description:In this work we show that neuromedin U receptor 1 (NMUR1)-mediated signaling programs SI eosinophils to support epithelial cell differentiation and barrier immunity. The global transcriptional profiling of eosinophils from different tissues of mice revealed that Nmur1 was expressed in a subset of eosinophils specifically in the SI. Fate mapping analyses showed that NMUR1 expression in SI eosinophils was imprinted by local microenvironment and further enhanced by the inflammation. Genetic deletion of NMUR1 decreased the numbers of eosinophils, degranulation activity, and goblet cell differentiation in the SI. Chemogenetic manipulation of NMU-expressing cells significantly altered the goblet cell differentiation and mucus secretion. Eosinophil-organoid co-culture experiments demonstrated that NMU-mediated eosinophil activation directly promoted the growth of intestinal organoids and formation of budding domains and complex crypt–villus structures. Finally, the deficiency of NMUR1 compromised anti-parasite immunity. Thus, NMU regulates epithelial cell differentiation and function through stimulating NMUR1-expressing eosinophils in the SI, highlighting the importance of neuro-immune-epithelium crosstalk in maintaining tissue homeostasis.
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Project description:The paper describes a model of immunity to melanoma.
Created by COPASI 4.25 (Build 207)
This model is described in the article:
Modeling anti-tumor Th1 and Th2 immunity in the rejection of melanoma
Raluca Eftimie, Jonathan L. Bramson, David J.D. Earn
Journal of Theoretical Biology 265 (2010) 467–480
Abstract:
Recent experiments indicate that CD4+ Th2 cells can reject skin tumors in mice, while CD4+ Th1 cells cannot (Mattes et al., 2003; Zhang et al., 2009). These results are surprising because CD4+ Th1 cells are typically considered to be capable of tumor rejection. We used mathematical models to investigate this unexpected outcome. We found that neither CD4+ Th1 nor CD4+ Th2 cells could eliminate the cancer cells when acting alone, but that tumor elimination could be induced by recruitment of eosinophils by the Th2 cells. These recruited eosinophils had unexpected indirect effects on the decay rate of type 2 cytokines and the rate at which Th2 cells are inactivated through interactions with cancer cells. Strikingly, the presence of eosinophils impacted tumor growth more significantly than the release of tumor-suppressing cytokines such as IFN-g and TNF-a. Our simulations suggest that novel strategies to enhance eosinophil recruitment into skin tumors may improve cancer immunotherapies.
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2024-09-02 | BIOMD0000000768 | BioModels
Project description:To determine how eosinophils adapt to the intestinal environment, eosinophils were sorted from the bone marrow and small intestine and compared by RNA sequencing. We show here that intestinal eosinophils were specifically adapted to their environment and underwent substantial transcriptomic changes. Intestinal eosinophils upregulated genes relating to the immune response and cell-cell communication, extracellular matrix components and metalloproteases, and the aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor with broad functions in intestinal homeostasis.
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Project description:Gene expression profiling of bone marrow derived eosinophils from miR-223 wildtype or miR-223 deficient mice
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Project description:A leading cause of morbidity and mortality during influenza infection is the development of a secondary bacterial pneumonia, which is appropriately treated with antibiotics. In the absence of a bacterial superinfection, prescribing antibiotics is not indicated but has nevertheless become a common clinical practice for those presenting with a respiratory viral illness. We found that antibiotic use during an antecedent influenza infection impaired the lung innate immunologic defenses toward a secondary challenge with methicillin-resistantStaphylococcus aureus(MRSA). The antibiotics perturbed the gut microbiome causing a fungal dysbiosis that drives an increase in lung eosinophils. We also demonstrate eosinophils, through the release of major basic protein, impair macrophage ability to clear MRSA. Moreover, we provide clinical evidence that eosinophils positively correlate with antibiotic use and worsened outcomes in patients hospitalized for viral infections. Altogether, our work establishes a counterproductive effect of antibiotic treatment during influenza infection that have negative immunologic consequences in the lungs thereby increasing the risk of developing a secondary bacterial infection.
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Project description:The eosinophil transcriptome analysis indicated a robust transcription change in eosinophils following allergen challenge in the lung. Eosinophils were FACS-sorted from Saline or OVA challenged lung with high purity and then subjected to genome-wide RNA microarray
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