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Updated: Mar 20, 2026
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Published on: June 2, 2022
Evidence of a pathogenic role for CD8(+) T cells in anti-GABAB receptor limbic encephalitis
Kristin S Golombeck1, Kathrin Bönte1, Constanze Mönig1
1Departments of Neurology (K.S.G., K.B., C.M., M.H., H.W., S.G.M., H.L., C.C.G., N.M.) and Clinical Radiology (W.S.), and Institute of Physiology I-Neuropathophysiology (S.G.M.), University of Münster; Departments of Epileptology (G.W., C.E.E.) and Neuropathology (K.M.v.L., A.J.B.), University of Bonn; Epilepsy Center Hamburg (M.L.), Evangelisches Krankenhaus Alsterdorf, Hamburg; and Department of Neuropathology (M.G.), University of Hamburg, Germany.
Objectives:
To characterize the cellular autoimmune response in patients with γ-aminobutyric acid (GABA)B receptor antibody-associated limbic encephalitis (GABAB-R LE).
Methods:
Patients underwent MRI, extensive neuropsychological assessment, and multiparameter flow cytometry of peripheral blood and CSF.
Results:
We identified a series of 3 cases of nonparaneoplastic GABAB-R LE and one case of paraneoplastic GABAB-R LE associated with small cell lung cancer. All patients exhibited temporal lobe epilepsy, neuropsychological deficits, and MRI findings typical of LE. Absolute numbers of CD19(+) B cells, CD138(+) CD19(+) plasma cells, CD4(+) T cells, activated HLADR(+) CD4(+) T cells, as well as CD8(+) T cells and HLADR(+) CD8(+) T cells did not differ in peripheral blood but were elevated in CSF of patients with GABAB-R LE compared to controls. Augmented absolute numbers of CD138(+) CD19(+) plasma cells and activated HLADR(+) CD8(+) T cells in CSF corresponded to higher overall neuropsychological and memory deficits in patients with GABAB-R LE. A histologic specimen of one patient following selective amygdalohippocampectomy revealed perivascular infiltrates of CD138(+) plasma cells and CD4(+) T cells, whereas cytotoxic CD8(+) T cells were detected within the brain parenchyma in close contact to neurons.
Conclusion:
Our data suggest a pathogenic role for CD8(+) T cells in addition to the established role of plasma cell-derived autoantibodies in GABAB-R LE.
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