Fig 4. Mitochondrial dysfunction in autoimmune adaptive immune cells.

(A) Glutamine metabolism enhances mitochondrial function in B cells fueling autoreactive plasmablast generation. (B) Enhanced mROS promote mitochondrial antiviral signaling protein (MAVS) activation and induction of type I IFN pathway; it also reduces T cell death, fueling inflammation. Dysfunctional mitochondria due to deficient NAD⁺ and aspartate production by mitochondria have been reported in inflammatory T cells infiltrating joints in patients with RA. The excessive mROS affects mito-translation, contributing to the pathologic cycle of mitochondrial dysfunction. In this environment, regulatory T-cell generation is impaired. Figure prepared using Biorender’s templates. IFN, interferon; mROS, mitochondrial reactive oxygen species; NAD, nicotinamide adenine dinucleotide; RA, rheumatoid arthritis.