Basal ganglia encephalitis (BGE) is poorly understood and associated with neurologic and neuropsychiatric sequelae of group A streptococcal (GAS) infections. For the first time, we identify immune subtypes of BGE and separate their neurologic sequelae associated with GAS or upper respiratory tract infections. Post-infectious BGE subtypes include the GAS sequelae Sydenham chorea (SC) and pediatric autoimmune neuropsychiatric disorder associated with streptococcal infections (PANDAS). Specifically, we identify the first human monoclonal (mAbs) from PANDAS and demonstrate that PANDAS autoantibodies (AAbs) activate the dopamine receptor 1 (D1R) in neuropsychiatric syndromes and dopamine receptor 2 (D2R) in choreiform movement disorders, separating the symptoms based on the DR AAb target. Subtypes were identified using novel BGE-derived human mAbs and patient serum autoantibodies. We report a novel mechanism for behavioral dysfunction in post-infectious neuropsychiatric sequelae in PANDAS/BGE where cross-reactive autoantibodies from GAS target D1R and lead to dopaminergic signaling abnormalities and drug-like enhancement of GPCR activity. Agonistic D1R autoantibody signaling was inhibited by D1R peptide epitopes derived from human D1R extracellular loops. Further, GAS-GlcNAc epitope carbohydrate antigen AAbs were elevated in PANDAS/BGE and inhibited binding of D1R demonstrating cross-reactivity. Human mAbs selectively targeted and activated dopamine receptors distinct from small-molecule agonists. Our work demonstrates the importance of the correct identification of BGE entities in order to treat GAS-positive cases or with appropriate antibiotics or immunomodulatory therapies. Our discovery contributes to the basic understanding of the autoimmune GAS sequelae that target the basal ganglia and furthers understanding of autoantibody GPCR signaling mechanisms, diagnosis, and treatment of autoimmune neuropsychiatric vs movement syndromes.