Authors :
Presenting Author: Nikki Gordon, MSc – Hadassah Hebrew University Medical Center Jerusalem Israel
Ariel Rechtman, MSc – Hadassah Hebrew University Medical Center Jerusalem Israel
Adi Vaknin-Dembinsky, MD, PhD – Hadassah Hebrew University Medical Center Jerusalem Israel
Dana Ekstein, Dr. – Hadassah Medical Center
Rationale:
Immune mechanisms have been proposed to underlie epileptic activity, but the knowledge on the precise immune processes in humans is limited. High levels of soluble CD83 (sCD83), a potentially immune-suppressive protein, have been linked to better response to immunomodulation in Myelin Oligodendrocyte Glycoprotein antibody-associated disease (MOGAD), an immune-mediated disease of the CNS. The current pilot study begins to investigate the potential role of sCD83 in epilepsy.
Methods:
We used NanoString technology on purified mRNA from peripheral blood monocytes (PBMCs) to determine mRNA expression in 5 patients with monophasic MOGAD and 3 with relapsing MOGAD, one of them also having epilepsy. ELISA protein assay was utilized to determine sCD83 concentrations in the CSF of 6 patients with seizures (one with relapsing MOGAD), 10 patients with monophasic MOGAD and 12 patients with relapsing MOGAD.
Results:
CD83 mRNA expression was 10.9 times higher (p=0.04) in the patients with monophasic MOGAD than in those with relapsing MOGAD, including the patient with epilepsy. sCD83 CSF protein concentration was low in the patients with monophasic MOGAD (287.60 ± 299.80 pg/ml) and relapsing MOGAD (155.70 ± 103.00 pg/ml) and reached an average of 763 pg/ml (± 571.8) in the patients with seizures. Notably, the patient with seizures and relapsing MOGAD had a concentration of 52 pg/ml. Three of the 6 seizure patients had low sCD83 concentrations (average 17.4 ± 24.6 pg/ml) and 3 had high concentrations (average 940.8 ± 476.4 pg/ml). Interestingly, the patients with seizures and low sCD83 were younger (average age 23.7) and underwent lumbar punctures after first unprovoked seizures due to prolonged clinical and electrographical post-ictal periods, initially suspected to be part of infectious or immune-mediated diseases. The patients with seizures and high sCD83 were older (average age 51.7) and had drug-resistant epilepsy.
Conclusions:
Immune-suppressive mechanisms mediated through CD83 may have a bidirectional interplay with epilepsy, possibly being upregulated by frequent seizure activity and contributing to mitigation of postictal symptoms. Low sCD83 concentrations may, on the other hand, contribute to perpetuation of seizures and seizure-induced CNS dysfunction. Further studies in larger population of patients are needed to elucidate the precise role of this protein in epilepsy.
Funding: none