IMMUNE DISTURBANCES IN PATIENTS WITH EPILEPSY AND OPPORTUNITY OF IMMUNOMODULATION BY RECOMBINANT HUMAN IL-2

Abstract: the inflammation in epilepsy pathogenesis is the subjects of scientific discussion. Extensive evidence in favor of the inflammatory theory of epileptogenesis is obtained, according to which epilepsy is a consequence of specialty inflammation in the CNS connected with both the induction of convulsions and their progression. Special attention is paid to cytokines containing in plasma mostly because they are natural pro-convulsants, the markers of inflammation, increased level of which result in higher risk of seizures. Inflammatory factors and mediators such as IL-1 p и TNF can influence on neuron transmission of mediators and promote development of hyper synchronous in neurons and hyper excitation of the brain. The specific role of cytokines IL-1 p in epilepsy is discerning due to it expression in CNS in astrocytes and microglia as a factor of chronic inflammation in CNS. The aim of our study is to evaluate the dynamics of immunological parameters in patients with epilepsy (PE) during the treatment with rIL-2-medicament (Roncoleukinum®), cytokine drug of Interleukins series containing recombinant human Interleukin-2 (rIL-2), which is a structural and functional analog of the endogenous IL-2. The results of the research of specialties of system inflammation response in epileptic patients reveal the increased level of the inflammation markers in plasma and CNS (increased concentration and violation of balance of cytokines of IL-1 p family defined by decrease of RAIL-1 concentration and RAIL-1/IL-1 coefficient). We obtained the data on decrease of content of pro-inflammatory cytokine IL-8 and increase content of BDNF in PE as a result of rIL-2-medicament treatment. Changes of these immunological parameters correlated with clinical improvement of PE: reduction of seizure frequency and positive EEG changes. These results might be used to optimize treatment of PE due to modulation of inflammatory process and increase of neurotrophic factors production required for the processes of brain neuroplasticity and neurogenesis