Nat Commun: Type I interferon promotes the occurrence and development of patients with systemic lupus erythematosus

Systemic lupus erythematosus (SLE) is a recurrent autoimmune disease, for which there is currently a lack of biological indicators for monitoring and predicting the occurrence of the disease.

Type I interferon composed of IFN-α, IFN-β, IFN-ε, IFN-κ and IFN-ω is an effective pleiotropic cytokine with diverse immune functions.

Several gene products encoded by ISGs are related to the regulation of antiviral defense mechanisms and cell functions.

Transcriptome analysis of CD8+T and CD4+T cells in SLE patients and healthy controls

In this study, the researchers analyzed the transcriptome of CD4+ and CD8+ T cells and found that mitochondrial-derived genes and mitochondrial-related metabolic pathways were down-regulated in patients with high IFN expression.

Changes of mitochondria of CD8+ T cells in SLE patients

Mechanism studies have shown that these "SLE-like" states will increase the consumption of NAD+ in CD8+ T cells, resulting in a decrease in mitochondrial respiratory function and a decrease in cell viability, both of which can be restored by supplementing NAD+.

Schematic diagram of type I interferon regulating SLE

All in all, the results of the study revealed that type I interferon can promote the death of CD8+ T cells through metabolic reprogramming, and promote the pathogenesis of SLE.