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IMMUNOMETABOLISM

IFNs disrupt T cell metabolism in SLE

Nature Reviews Rheumatology volume 17, page 310 (2021)Cite this article

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Systemic lupus erythematosus (SLE) is often accompanied by increased expression of type I interferon (IFN)-stimulated genes (ISGs), commonly referred to as the type I IFN signature, that is strongly linked to disease activity. Emerging evidence also suggests that metabolic changes in immune cells, including mitochondrial abnormalities, contribute to immune dysregulation and SLE pathogenesis. New findings link chronic type I IFN signalling with mitochondrial abnormalities in CD8+ T cells in patients with SLE and provide further rationale for exploring metabolic pathways as therapeutic targets in this disease.

In searching for differentially expressed genes in the T cell signatures of patients with SLE versus healthy individuals, Buang et al. discovered an enrichment in mitochondrial-associated metabolic pathways, particularly in CD8+ T cells, that was linked to the expression of ISGs. They also identified various mitochondrial changes in the CD8+ T cells of patients with SLE that were associated with a high IFN signature, including an increase in mitochondrial size and membrane hyperpolarization and a reduced spare respiratory capacity. By contrast, the CD4+ T cells had no detectable changes in any of the mitochondrial parameters assessed.

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Original article

  • Buang, N. et al. Type I interferons affect the metabolic fitness of CD8+ T cells from patients with systemic lupus erythematosus. Nat. Commun. 12, 1980 (2021)

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

    Jessica McHugh

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  1. Jessica McHugh
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Correspondence to Jessica McHugh.

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McHugh, J. IFNs disrupt T cell metabolism in SLE. Nat Rev Rheumatol 17, 310 (2021). https://doi.org/10.1038/s41584-021-00622-1

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