Background & Objective: Epilepsy is one of the most complex neurological disorders and
its study requires a broad knowledge of neurology and neuroscience. It comprises a diverse group of
neurological disorders that share the central feature of spontaneous recurrent seizures, and are often
accompanied by cognitive deficits and mood disorder. This condition is one of the most common neurological
disorders. Until recently, alterations of neuronal activities had been the focus of epilepsy
research. This neurocentric emphasis did not address issues that arise in more complex models of
epileptogenesis. An important factor in epilepsy that is not regulated directly by neurons is inflammation
and the immune response of the brain. Recent evidence obtained in rodent epilepsy models supports
the role of immune responses in the initiation and maintenance of epilepsy. Recognition of exogenous
pathogens by the innate immune system is mediated by some pattern recognition receptors
such as Toll-like receptors leading to cell activation and cytokine production. Currently, these receptors
have been the focus of epilepsy studies looking to determine whether the innate immune activation
is neuroprotective or neurotoxic for the brain.
Conclusion: Here, we present the evidence in the literature of the involvement of key innate immune
receptors in the development of epilepsy. We address some of the contradictory findings in these studies
and also mention possible avenues for research into epilepsy treatments that target these receptors.