Autoantibodies elicited by prenatal maternal infections with Neisseria gonorrhoeae (N. gonorrhoeae) are suspected to play a role in the pathogenesis of neurodevelopmental diseases like schizophrenia. This chapter provides an overview on research about cellular interaction partners of such antibodies in choroid plexus epithelial cells. In a first set of experiments, it was revealed that antibodies to N. gonorrhoeae interact with mitochondrial proteins like Hsp60 and ATBP5, leading to impaired energy metabolism in choroid plexus papilloma cells. This interaction was confirmed in postmortem samples of the choroid plexus as well as in choroid plexus epithelium from Callithrix jacchus, a nonhuman primate. In a further set of experiments, employing a multiprotein array, it was shown that the interaction of anti-N. gonorrhoeae antibodies with the SNARE-protein Snap23 was capable of impairing the insulin-dependent membrane translocation of the glucose transporter GluT4 in choroid plexus papilloma cells. These findings show that antibacterial antibodies implicated in the etiology of schizophrenia are capable of interacting with certain proteins in the choroid plexus epithelium, which eventually leads to functional alterations that could play a role in the pathogenesis of this disease.