Immune landscape of the affected brain in Rasmussen encephalitis.

Overview

1. Department of Integrative Biology and Physiology, College of Life Sciences, University of California Los Angeles, Los Angeles, CA USA
2. Division of Neuropathology, Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA USA
3. Department of Neurology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA USA
4. Department of Radiological Sciences, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA USA
5. Department of Neurosurgery, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA USA

Abstract

Rasmussen encephalitis (RE) is a rare neuroinflammatory disease characterized by intractable seizures and progressive brain atrophy that is usually confined to one cerebral hemisphere. Disease management involves anti-seizure medications and immunotherapy, although surgical resection remains the only effective treatment option to achieve seizure freedom. The presence of clonally expanded resident memory T cells in brain tissue removed to control seizures suggests the involvement of an autoimmune response in the etiology of the disease. Blocks of fresh brain tissue were obtained from three RE surgery cases (ages 5, 8, and 26 years at the time of surgery) and immune cells were isolated. Single cell RNA sequencing was used to define the types of immune cells present in the affected brain tissue and potential crosstalk between them, along with multiplex immunofluorescence immunostaining of sections from the same specimens. We matched T cell receptor sequences to T cell phenotypes and used ViralTrack software to search for evidence of activation of latent viruses in the immune cells. The immune cells isolated from the three RE cases comprised primarily activated microglia and resident memory CD8 T cells with fewer CD4 T cells, NK cells and monocyte-derived macrophages and dendritic cells. The majority of CD8 T cells expressed killer cell lectin-like receptors, and a virus responsive gene signature that included XCL1, TNFRSF9 and CRTAM, but also the exhaustion markers LAG-3 and TIM-3. Microglia expressed transcripts found in disease-associated microglia and transcripts associated with NLRP3 inflammasomes. We found no evidence for active latent viruses; however, we found endogenous HERV-K retrovirus sequences that were transcribed from multiple provirus insertion sites.

Supplementary Information: The online version contains supplementary material available at 10.1038/s41598-026-51295-3.

Reproduced under the paper's license (CC BY), from the paper cited above.

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Data

Datasets cited

• geo:GSE312319, at NCBI GEO; found in “Data availability”

Data availability

NCBI Gene Expression Omnibus accession number GSE312319 (https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE312319).

Reproduced under the paper's license (CC BY), from the paper cited above.

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Version 1, 28 September 2026: the first record

Recorded: type, language, journal, volume, issue, pages, dates, 8 authors, 8 keywords, 11 MeSH terms, 4 funders, 138 references.

Cite

This paper

Quinones-Valdez, G., Chang, J. W., Magaki, S. D., Vinters, H. V., Salamon, N., Wang, A. C., Fallah, A., & Owens, G. C. (2026). Immune landscape of the affected brain in Rasmussen encephalitis. Scientific reports, 16(1), 21957. https://doi.org/10.1038/s41598-026-51295-3

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