CD8A and systemic lupus erythematosus: Targeted inhibition of CD38 in a murine lupus model restored CD8+ T cell effector function, enhanced mitochondrial quality via improved mitophagy, and bolstered viral clearance.[24] Similarly, type I interferon exposure in SLE downregulates mitochondrial genes and impairs mitochondrial metabolism in CD8+ T cells, leading to enlarged mitochondria, reduced spare respiratory capacity, and increased cell death upon TCR stimulation.