Adaptive immunity cells are differentially distributed in the peripheral blood of glycine receptor antibody-positive patients with focal epilepsy of unknown cause

•GlyR-Ab positive patients exhibited significantly increased CD3+CD4+CD25highregulatory T (Treg) cells and CD3+CD4+CD25highCD127low/- Treg cells and relatively increased CD19+IgD-CD27+ memory B cells without attaining statistical significance.•GlyR antibody positive patients showed differential blood immunophenotype distribution as compared to seronegative epilepsy patients and healthy controls, suggesting that GlyR antibody positive, focal epilepsy patients with an unknown cause have a distinct physiopathology.•Our study has provided clues suggesting that adaptive immunity might participate in some subgroups of focal epilepsy of unknown cause. Glycine receptor (GlyR) autoantibodies (Ab) have been recently detected in epilepsy patients. Our study aimed to investigate the peripheral blood distribution of B and T cell subgroups responsible for antibody production to find clues supporting the distinct organization of adaptive immunity in focal epilepsy of unknown cause (FEUC). Seven GlyR-Ab positive and 15 GlyR-Ab negative FEUC patients and 25 age-sex matched healthy individuals were included. Peripheral blood mononuclear cells were isolated and immunophenotyped by flow cytometry. There were no significant differences between CD19+ B, CD3+ T, CD4+ helper T, CD8+ cytotoxic T, and CD19+CD24++CD38++ regulatory B cell ratios among the groups. GlyR-Ab negative epilepsy patients had significantly higher CD19+IgD+CD27− naive B cells and GlyR-Ab positive patients showed reduced percentages of CD19+CD38+CD138+ plasma cells than healthy controls. By contrast, GlyR-Ab positive patients exhibited significantly increased CD3+CD4+CD25highregulatory T (Treg) cells and CD3+CD4+CD25highCD127low/- Treg cells and relatively increased CD19+IgD-CD27+ memory B cells without attaining statistical significance. The increase of Tregs, which are capable of suppressing B cells, maybe a compensating countermeasure to prevent the conversion of effector B cell subgroups. Thus, our findings lend support to the involvement of adaptive immunity in focal epilepsy of unknown cause.