The widespread availability of single-cell and single-nuclear genomic tools has enabled unbiased and high-dimensional assessment of tissue immunity in the kidney. The application of these technologies to human and mouse kidney samples, combined with spatial transcriptomics, has yielded unexpected insights into how resident and infiltrating immune cells maintain tissue homeostasis and drive disease.
Key advances
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Large-scale single-cell and single-nucleus RNA sequencing datasets of human kidney samples provide a rich community resource that can generate hypotheses and reveal potential treatment targets for validation and/or further investigation.
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The kidney is home to tissue-resident B cells in homeostasis that polarize local macrophages to an anti-inflammatory phenotype via IL-10 secretion.
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Ageing kidneys contain lymphocyte aggregates (tertiary lymphoid structures) adjacent to damaged proximal tubules; these lymphocytes produce cytokines that can sustain and amplify local inflammation.
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In anti-neutrophil cytoplasmic antibody-associated vasculitis, CD4 T cells in the kidney produce granulocyte–macrophage colony-stimulating factor, stimulating macrophage production of metalloproteinase 12, which has the potential to damage basement membrane components.
References
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Yoshikawa, T. et al. Tertiary lymphoid tissues are microenvironments with intensive interactions between immune cells and proinflammatory parenchymal cells in aged kidneys. J. Am. Soc. Nephrol. 34, 1687–1708 (2023).
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Paust, H. J. et al. CD4+ T cells produce GM-CSF and drive immune-mediated glomerular disease by licensing monocyte-derived cells to produce MMP12. Sci. Transl. Med. 15, eadd6137 (2023).
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Stewart, A.P., Clatworthy, M.R. Single-cell genomics sheds light on kidney tissue immunity. Nat Rev Nephrol 20, 71–72 (2024). https://doi.org/10.1038/s41581-023-00802-0
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DOI: https://doi.org/10.1038/s41581-023-00802-0
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