Neuropsychiatric diseases associated with infections, including those triggered by Group A Streptococcus (GAS), remain a major, unresolved global health issue. GAS infections can lead to autoimmune sequelae, manifesting as movement disorders such as Sydenham chorea and neuropsychiatric symptoms. Despite increasing recognition of these diseases, their molecular mechanisms are not fully understood. Our previous research has shown that autoantibodies (AAbs) targeting dopaminergic neurons can enhance dopamine D2 receptor (D2R) signaling. However, the role of AAbs in modulating dopamine D1 receptor (D1R) activity remains less explored. We demonstrate that GAS-induced cross-reactive AAbs contribute to autoimmune encephalitis of the basal ganglia, a brain region rich in dopamine receptors. Specific differences in D1R and D2R AAb titers, receptor signaling, receiver operating characteristic curves, and immunoreactivity to D1R and D2R autoreactive epitopes can distinguish neuropsychiatric syndromes from movement disorders. Notably, affected individuals exhibit elevated and abnormal AAb responses to the GAS Group A carbohydrate epitope, N-acetylglucosamine (GlcNAc), and increased Th17 cytokines, indicative of dysregulated immune responses. D1R AAb signaling was observed using both patient serum-derived AAbs and novel patient-derived monoclonal antibodies (mAbs), which induced G protein- and β-arrestin-mediated D1R signaling. Moreover, these patient AAbs and mAbs enhanced D1R signaling through dopamine-dependent pathways. These findings suggest that AAb-mediated D1R signaling, alongside aberrant GlcNAc-reactive AAbs and Th17 cytokine elevations, plays a pivotal role in the pathogenesis of neuropsychiatric sequelae, offering potential diagnostic and therapeutic avenues for GAS-associated sequelae and related neuropsychiatric disorders.