# Microvascular immunity is organ-specific and remodeled after kidney injury in mice

**Authors:** Rebecca Rixen, Paula Schütz, Carolin Walter, Birte Hüchtmann, Veerle Van Marck, Barbara Heitplatz, Julian Varghese, Georg Varga, Dirk Foell, Thomas Pap, Hermann Pavenstädt, Konrad Buscher

PMC · DOI: 10.1038/s41467-025-59609-1 · Nature Communications · 2025-05-09

## TL;DR

The study shows that immune cells in the microvasculature of organs like the kidney change uniquely after injury, revealing new insights into immune responses.

## Contribution

The paper introduces the concept of organ-specific immune cell dynamics in the microvasculature following kidney injury.

## Key findings

- Immune cells in the kidney vasculature expand up to 100-fold after injury, including macrophages and B cells.
- Renal microvascular regeneration involves new macrophage subsets with enhanced phagocytic activity.
- Microvascular immune changes after AKI are not detectable through conventional blood or tissue analysis.

## Abstract

Many studies analyze tissue-resident or blood-borne leukocytes to monitor disease progression. We hypothesized that the microvasculature serves as a distinct site for immune cell activity. Here, we investigate microvascular leukocyte phenotypes before, during and after acute kidney injury (AKI) in mice, uncovering unique characteristics in the kidney, liver, and lung. Using single-cell sequencing, we identify several immune cells that were up to 100-fold expanded in the kidney vasculature, including macrophages, dendritic cells (DC), and B cells. Regeneration after AKI is characterized by sustained remodeling of the renal microvascular interface. Homeostatic microvascular C1q+ macrophages withdraw from the vascular barrier which is subsequently repopulated by new subsets, including CD11c+F480+ and CD11c+F480− cells. These newly arrived macrophages exhibit enhanced phagocytic activity toward circulating bacteria and secretion of tumor necrosis factor, pointing to maladaptive repair mechanisms after AKI. These data suggest organ- and disease-specific microvascular immune dynamics which are not detectable through conventional blood and tissue analysis.

During tissue injury blood cells in the microvasculature and tissue resident cells have differing phenotypes. Here the authors use single cell transcriptomics in mice models to assess the differences in phenotype of immune cells in multiple organs and the tissue resident cells before, after and during acute kidney infection.

## Linked entities

- **Proteins:** C1qa (complement component 1, q subcomponent, alpha polypeptide)
- **Diseases:** acute kidney injury (MONDO:0002492), AKI (MONDO:0002492)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** Adgre1 (adhesion G protein-coupled receptor E1) [NCBI Gene 13733] {aka DD7A5-7, EGF-TM7, Emr1, F4/80, Gpf480, Ly71}, C1qa (complement component 1, q subcomponent, alpha polypeptide) [NCBI Gene 12259] {aka Adic, C1q}, Tnf (tumor necrosis factor) [NCBI Gene 21926] {aka DIF, TNF-a, TNF-alpha, TNFSF2, TNFalpha, Tnfa}, Itgax (integrin alpha X) [NCBI Gene 16411] {aka Cd11c, Cr4, N418}
- **Diseases:** AKI (MESH:D058186), kidney injury (MESH:D007674)
- **Species:** Mus musculus (house mouse, species) [taxon 10090]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12064663/full.md

## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12064663/full.md

## References

4 references — full list in the complete paper: https://tomesphere.com/paper/PMC12064663/full.md

---
Source: https://tomesphere.com/paper/PMC12064663