Limbic encephalitis (LE) is increasingly recognized as a possible cause of chronic temporal lobe epilepsy (TLE). Key aspects of such a transient inflammation in the limbic system are still largely enigmatic. We use a combination of complementary state-of-the-art cell culture, animal model and human TLE biomaterial experimental approaches. We examine the functional consequences of exposure of primary neuronal cell cultures to several LE-relevant autoantibodies as well as to new auto-antibodies recently detected in our screens of LE-TLE patient biofluids. Overall, this project will contribute to an improved understanding of the pathogenesis of LE and result in better diagnostic and therapeutic regimens for affected patients.