Inhibición de ROS mitocondriales por TACI sostiene las células plasmáticas de la médula ósea

cell-independent antigens. Importantly, TACI deficiency severely compromises protection elicited by both SARS-CoV-2 and influenza vaccines. Mechanistically, loss of TACI causes accumulation of mitochondrial reactive oxygen species and subsequent plasma cell death. Importantly, pharmacologic antioxidant treatment with the FDA-approved drug, N‑acetylcysteine, mitigates ROS accumulation, rescues LLPC numbers, and enhances influenza vaccine efficacy in vivo. Together, these results establish TACI as a non-redundant regulator of LLPC longevity and vaccine-induced protection by limiting oxidative stress, providing a potential