Long COVID postural orthostatic tachycardia syndrome affects immune cell function through a cascade of oxidative stress in monocytes. Researchers found threefold higher levels of T cell-monocyte doublets in 25 LCPOTS patients compared to 15 recovered controls, with these immune complexes producing elevated inflammatory cytokines IFN-gamma and IL-17A. The monocytes showed increased mitochondrial superoxide generation and accumulation of isolevuglandin adducts, markers of oxidative damage, while expressing fewer antioxidant genes. This oxidative environment creates a feedback loop where impaired cardiovascular regulation stimulates reactive oxygen species production, which then forms neoantigens that activate more T cells. The severity of immune activation correlated directly with heart rate abnormalities and symptom burden. This mechanism helps explain why Long COVID POTS involves both cardiovascular dysfunction and widespread inflammatory symptoms affecting energy, cognition, and multiple organ systems. The findings suggest antioxidant interventions might interrupt this cycle, though this preprint awaits peer review and the sample size was modest. Understanding this oxidative-immune axis represents a significant step toward targeted therapies for the estimated millions suffering from Long COVID's cardiovascular complications.