Single cell analysis identifies the key role of basophils orchestrating Th17 immunity and kidney fibrosis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA755599 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15500516.fastq.gz | Fastqsanger.gz | |||
| SRR15500517.fastq.gz | Fastqsanger.gz | |||
| SRR15500518.fastq.gz | Fastqsanger.gz | |||
| SRR15500519.fastq.gz | Fastqsanger.gz | |||
| SRR15500520.fastq.gz | Fastqsanger.gz |
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Project description:Inflammation is a key component of fibrosis, however, the immune processes that orchestrate kidney fibrosis are poorly understood. By performing single-cell sequencing of a mouse model of kidney fibrosis, we identified a subset of kidney tubule cells with a profibrotic-inflammatory phenotype, characterized by the expression of cytokines and chemokines associated with immune cell recruitment. Receptor-ligand interaction analysis and experimental validation indicated that CXCL1 secreted by profibrotic tubules recruits CXCR2+ basophils. In mice, these basophils were the key source of IL-6 and were responsible for the recruitment of Th17 cells. Genetic deletion or antibody-based depletion of basophils resulted in reduced renal fibrosis. Human kidney single-cell, bulk gene expression, and immunostaining results validated the role of basophils in patients with kidney fibrosis. Collectively, these studies identify basophils as key contributors to the development of renal fibrosis and suggest that targeting these cells may be a useful strategy for the management of chronic kidney disease.
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2013-04-01 | E-GEOD-41596 | biostudies-arrayexpress
Project description:Inflammation is an important component of fibrosis but immune processes that orchestrate kidney fibrosis are not well understood. Here we apply single-cell sequencing to a mouse model of kidney fibrosis. We identify a subset of kidney tubule cells with a profibrotic-inflammatory phenotype characterized by the expression of cytokines and chemokines associated with immune cell recruitment. Receptor-ligand interaction analysis and experimental validation indicate that CXCL1 secreted by profibrotic tubules recruits CXCR2+ basophils. In mice, these basophils are an important source of interleukin-6 and recruitment of the TH17 subset of helper T cells. Genetic deletion or antibody-based depletion of basophils results in reduced renal fibrosis. Human kidney single-cell, bulk gene expression and immunostaining validate a function for basophils in patients with kidney fibrosis. Collectively, these studies identify basophils as contributors to the development of renal fibrosis and suggest that targeting these cells might be a useful clinical strategy to manage chronic kidney disease.
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Project description:Human basophils regulate allergic immune responses by releasing histamine and effector cytokines such as interleukin 4 (IL-4) and IL-13. IL-3/IL-3R signaling axis plays key roles in the maturation, survival and activation of basophils. We and others have shown that IL-3-induced surface receptors e.g. ST2 and IL-17RB regulate the biology of basophils. We in this study aim to identify new basophil activation maker and regulator by transcriptomic analysis of IL-3-stimulated basophils.
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Project description:To investigate the mechanisms by which C/EBPa drives basophil differentiation and maintains basophil identity, we examined whether or not C/EBPa promotes basophil molecular programming and simultaneously represses mast cell molecular programming. We performed genome-wide gene expression profiling on basophils and mast cells and found that 6798 genes were shared by mast cells and basophils; 2033 genes were expressed 2-10 (log2 1-3.3)-fold higher in basophils (differentially expressed in basophils); and 413 genes were expressed greater than 10 (log2 3.3)-fold in basophils (highly expressed in basophils). On the other hand, we found 569 genes were expressed 2-10 (log2 -1 to -3.3) fold higher in mast cells and 171 genes were highly expressed in mast cells [greater than 10 fold (log2 -3.3)]. We treated purified basophils prepared from Cebpaf/f RosaYFP/creER mice and Cebpa+/+ RosaYFP/creER control mice with or without 4HT treatment for five days. Gene expression in the treated basophils was analyzed using microarray analysis. Overall, deletion of C/EBPa in basophils resulted in a reduction of mRNA expression for 248 genes and led to an increase in mRNA expression for 255 genes. The majority of the C/EBPa-regulated genes were either differentially or highly expressed in basophils or mast cells.
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