The first meeting on Immunity and Inflammation in Epilepsy overviewed and discussed the current knowledge in this field of experimental and clinical research with the principal aim of identifying areas of further investigations to address the still unresolved fundamental aspects. The interdisciplinary group of basic science and clinical investigators proposed preliminary answers to the identified crucial questions, as summarized in Table 1. The possible causes of brain inflammation were discussed in the frame of different epilepsy etiologies. The role of recurrent seizures per se as a cause of persistent inflammation, beyond a detectable structural insult, was highlighted. However, the identification of contributing factors to the inflammatory process and their clinical relevance are still largely unknown. The contribution of brain inflammation to hyperexcitability underlying seizures is well delineated in experimental models, although the role of inflammatory mediators in epileptogenesis requires additional studies. Aspects awaiting further investigations include: (1) the discovery and characterization of novel inflammatory molecules and pathways in multiple experimental models; (2) elucidating whether and how the inflammatory pathways so far identified converge into common molecular targets; (3) the validation of inflammatory processes described in the experimental setting in surgically resected epileptogenic tissue from epilepsies of different etiology; and (4) development of strategies to target these inflammatory factors in order to inhibit seizures and/or prevent epileptogenesis. Major challenges include exploring cellular, molecular, and genetic mechanisms that may contribute to seizures and comorbidities in immune-mediated epilepsies, and establishing disease-specific animal models, as has been done for tuberous sclerosis complex or Dravet syndrome. The elucidation of the specific bystander (association) or truly causative role of autoantibodies present in several epileptic syndromes and autoimmune disorders may also improve management (diagnosis, treatment, and long-term disease monitoring) of patients with these conditions. International disease-specific consortia will help to identify and recruit numbers of patients with the still very rare autoimmune epilepsy syndromes, sufficient to fulfil the criteria for well-designed clinical trials. Systematic collection of clinical information and biologic samples that take into account the possible immune or inflammatory aspects of the epileptic condition, the development of noninvasive techniques to image brain inflammation, and the identification of biomarkers of brain inflammation in cerebrospinal fluid (CSF) and blood will greatly improve the identification of patients who may best benefit from a specific immunosuppressant or antiinflammatory treatment. Proof-of-concept pharmacologic evidence in experimental models may contribute to the discovery of new compounds, or to the identification of drugs already used for other clinical indications (e.g., in chronic inflammatory diseases), which may be considered for prospective clinical trials for treating seizures in autoimmune-mediated epilepsies, and more in general for the treatment of seizures that are not controlled by classical antiepileptic drugs (AEDs) in nonimmune types of epilepsies. Future meetings and multidisciplinary collaborations between basic science and clinical research with translational purposes will reinforce the efforts of gaining further insights into the complex role of immunity and inflammation in epilepsy, and hopefully will encourage the development of new treatments with disease-modifying therapeutic potential. A. Vezzani and S. Rüegg thank the scientific committee, the speakers, and the discussants. They are especially grateful to the Commission of European Affair of ILAE; the American Epilepsy Society; UCB Pharma, Basel, Switzerland; Sanofi-Aventis, Milano, Italy; and Questcor Union City, CA, U.S.A. for their support, which was instrumental for the realization of this meeting. We thank Philip Schwarzkroin and Simon Shorvon for providing us the opportunity to publish the proceedings of this meeting in Epilepsia.