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Autoimmunity

Mito+ RBCs prompt IFN and IL-1β release by SLE monocytes

Nature Reviews Rheumatology volume 20, page 742 (2024)Cite this article

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In some individuals with systemic lupus erythematosus (SLE), red blood cells retain their mitochondria (Mito+ RBCs), and internalization of Mito+ RBCs by macrophages triggers the production of type I interferon. Findings now identify a subset of monocytes, which are expanded in active SLE, that internalize Mito+ RBCs and subsequently express interferon-stimulated genes, leading to IL-1β production via an unconventional secretory pathway.

The researchers found that the expression of type I interferon in this subset of monocytes was dependent on the sensing of both mitochondrial DNA (mtDNA, mediated by cGAS) and mitochondrial RNA (mtRNA, mediated by RIG-I receptors (RLRs)). The sensing of mtRNA from internalized Mito+ RBCs via the RLR antiviral signalling adaptor pathway also induced the production of IL-1β in these cells, by triggering the cytosolic release of monocyte mtDNA that activates the NLRP3 inflammasome.

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  1. Nature Reviews Rheumatology http://www.nature.com/nrrheum/

    Holly Webster

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  1. Holly Webster
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Correspondence to Holly Webster.

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Webster, H. Mito+ RBCs prompt IFN and IL-1β release by SLE monocytes. Nat Rev Rheumatol 20, 742 (2024). https://doi.org/10.1038/s41584-024-01183-9

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  • DOI: https://doi.org/10.1038/s41584-024-01183-9

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