These effects are linked to elevated NAD+ consumption and impaired mitochondrial respiration, which can be rescued by NAD+ supplementation, highlighting a potential mechanism by which type I IFN contributes to CD8+ T cell dysfunction in SLE.[25] In primary Sjogren's syndrome, immune cell populations in labial salivary glands exhibit distinct associations with mitochondrial pathways. Here, CD8A is linked to systemic lupus erythematosus.