Abstract | PURPOSE: The expression of the major histocompatibility complex class I (MHC-I) in the brain has received considerable interest not only because of its fundamental role in the immune system, but also for its non-immune functions in the context of activity-dependent brain development and plasticity. METHODS: RESULTS: All lesions were characterized by MHC-I expression in blood vessels. Expression in both endothelial and microglial cells as well as in neurons (dysmorphic/dysplastic neurons) was observed in FCD II, TSC and GG cases. We observed perivascular and parenchymal T lymphocytes (CD8+, T-cytotoxic) with granzyme-B+ granules in FCD IIb and TSC specimens. Albumin extravasation, with uptake in astrocytes, was observed in FCD IIb and GG cases. CONCLUSIONS: Our findings indicate a prominent upregulation of MHC-I as part of the immune response occurring in epileptogenic glioneuronal lesions. In particular, the induction of MHC-I in neuronal cells appears to be a feature of type II FCD, TSC and GG and may represent an important accompanying event of the immune response, associated with blood-brain barrier dysfunction, in these developmental lesions.
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Authors | Avanita S Prabowo, Anand M Iyer, Jasper J Anink, Wim G M Spliet, Peter C van Rijen, Eleonora Aronica |
Journal | Journal of neuroinflammation
(J Neuroinflammation)
Vol. 10
Pg. 12
(Jan 24 2013)
ISSN: 1742-2094 [Electronic] England |
PMID | 23347564
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Topics |
- Adolescent
- Adult
- Aged
- Child
- Child, Preschool
- Female
- Gene Expression Regulation
(immunology)
- Genes, MHC Class I
(immunology)
- Humans
- Major Histocompatibility Complex
(immunology)
- Male
- Microglia
(immunology, metabolism, pathology)
- Neurons
(immunology, metabolism, pathology)
- Tuberous Sclerosis
(immunology, metabolism, pathology)
- Young Adult
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