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INNATE IMMUNITY

APOL1 variants contribute to racial disparity in sepsis

Nature Reviews Immunology volume 21, page 759 (2021)Cite this article

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Individuals of African ancestry are more likely to die from sepsis than individuals of European ancestry and are also disproportionately affected by COVID-19, with both higher infection rates and more severe disease. A study published in Immunity suggests that genetic variants in apolipoprotein L1 (APOL1) contribute to this susceptibility, by affecting mitophagy in endothelial cells and allowing the release of mitochondrial DNA (mtDNA) that activates inflammasome and nucleotide sensing pathways.

To explore the role of APOL1 in endothelial dysfunction, the authors generated mice in which expression of a human APOL1 risk allele (G2APOL1) or wild-type allele is induced specifically in endothelial cells. Endothelial expression of G2APOL1 was associated with loss of glomerular capillary fenestrations and delamination of alveolar capillaries, and led to increased vascular permeability. Moreover, transcripts for endothelial glycocalyx remodelling (an indicator of endotheliopathy), vascular inflammation and adhesion were upregulated in mice expressing G2APOL1.

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  1. Nature Reviews Immunology http://www.nature.com/nri/

    Lucy Bird

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  1. Lucy Bird
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Correspondence to Lucy Bird.

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Bird, L. APOL1 variants contribute to racial disparity in sepsis. Nat Rev Immunol 21, 759 (2021). https://doi.org/10.1038/s41577-021-00647-3

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  • DOI: https://doi.org/10.1038/s41577-021-00647-3

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