“…In particular, high levels of proinflammatory cytokines [e.g., interleukin-1beta (IL-1β), tumor necrosis factor-alpha (TNFα)], damage signals [high-mobility group box 1 (HMGB1), S100 beta] and downstream inflammatory mediators (e.g., prostaglandins, the complement system) have been measured in epileptogenic tissue from patients affected by epilepsy of various etiologies (Aronica and Crino, 2011; Vezzani et al, 2011). The major contributors to the synthesis of these inflammatory mediators are brain-resident cells such as activated microglia, astrocytes, and neurons (Devinsky et al, 2013), but also systemic invading leukocytes play an important role in epileptogenesis, particularly when the permeability of the blood-brain barrier is alterated (Fabene et al, 2008; Deprez et al, 2011). …”