AI Article Synopsis

  • Inflammation plays a key role in kidney fibrosis, yet the immune processes behind it are not fully understood, prompting researchers to use single-cell sequencing in a mouse model.
  • They discovered a unique group of kidney tubule cells that produce cytokines and chemokines, which attract immune cells like basophils, particularly through the secretion of CXCL1.
  • The study shows that basophils are crucial for inducing interleukin-6 and recruiting specific helper T cells, with findings in mice suggesting that targeting these cells could help treat chronic kidney disease.

Article Abstract

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 T17 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.

Download full-text PDF

Source
http://dx.doi.org/10.1038/s41590-022-01200-7DOI Listing

Publication Analysis

Top Keywords

kidney fibrosis
16
renal fibrosis
8
kidney
7
fibrosis
7
basophils
6
single-cell analysis
4
analysis identifies
4
identifies interaction
4
interaction altered
4
altered renal
4

Similar Publications

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!