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CD19+ B-cells in autoantibody-negative limbic encephalitis

Niels Hansen1, Demet Önder2, Kerstin Schwing2

  • 1Department of Epileptology, University of Bonn Medical Center, Venusberg - Campus 1, 53127 Bonn, Germany; Department of Psychiatry and Psychotherapy, University Medicine Goettingen, Von-Siebold-Str. 5, 37075 Goettingen, Germany.

Epilepsy & Behavior : E&B
|March 22, 2020
PubMed

Insights

Increased CD19+ B-cells in cerebrospinal fluid (CSF) and blood-brain barrier impairment are observed in antibody-negative limbic encephalitis (LE). Further research is needed to understand the role of these B-cells in central nervous system (CNS) immunity and treatment strategies.

Area of Science:

  • Neuroimmunology
  • Cellular immunology
  • Epileptology

Background:

  • Temporal lobe epilepsy (TLE) can be caused by limbic encephalitis (LE), a condition with varying immunological profiles.
  • Understanding the immune mechanisms in different LE subtypes is crucial for targeted therapies.

Purpose of the Study:

  • To investigate the cellular immune repertoire in patients with TLE due to LE, differentiating between antibody-negative and antibody-associated LE.
  • To explore the potential of flow cytometry in identifying biomarkers for subtype-specific treatment strategies.

Main Methods:

  • Flow cytometry was used to analyze peripheral blood (PB) and cerebrospinal fluid (CSF) immune cells in 62 TLE patients with LE.
  • Patients were categorized into antibody-negative LE (n=40) and neural autoantibody-positive LE (n=22).
  • Neuropsychological testing, MRI, and EEG were also performed.

Main Results:

  • CD19+ B-cells were significantly elevated in the PB and CSF of antibody-negative LE patients compared to those with intracellular antibody-positive LE.
  • Impaired blood-brain barrier function was more prevalent in antibody-negative LE.
  • No significant differences were found in other measured immune cell subsets (CD138+, CD4+, CD8+, HLA-DR+ cells) between LE groups.

Conclusions:

  • Elevated CD19+ B-cells and blood-brain barrier dysfunction in antibody-negative LE suggest their involvement in the disease.
  • The exact pathogenic role of these B-cells in central nervous system (CNS) immunity remains unclear due to a lack of correlation with clinical parameters.
  • Further studies are warranted to assess the utility of CD19+ B-cells as biomarkers for treatment stratification in LE.
Abstract

Keywords:
AutoimmunityB-cellsLimbic encephalitisNeural antibodiesT-cellsTemporal lobe epilepsy

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