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Epilepsy Behav. 2007 Feb;10(1):206-11. Epub 2006 Oct 27.

Rasmussen's encephalitis: interleukin-10-dependent Tc2 cell polarization may explain its pathophysiology and clinical course.

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1
Department of Neurology and Comprehensive Epilepsy Center, University of Kansas Medical Center, Kansas City, KS, USA. iosorio@kumc.edu

Abstract

Little is known about the cellular immune dynamics and pathophysiology of Rasmussen's encephalitis (RE). We investigated transcriptional expression of pro- and anti-inflammatory cytokines and characterized the T-cell subset types present in temporal and frontal lobe specimens obtained from a child with RE. Interleukin (IL)-10 and macrophage scavenger receptor type I mRNA assessed by semiquantitative reverse transcription polymerase chain reaction was found in temporal but not in affected frontal lobe tissue. Messenger RNA specific to tumor necrosis factor alpha, IL-l, IL-4, IL-6, IL-12, IL-15, IL-18, transforming growth factor beta, CD-14, and inducible nitric oxide synthase was not detected in either temporal or frontal tissue with histopathologically manifest evidence of disease. Virtually all lymphocytic infiltrate consisted of CD3+ CD8+ T cells. We speculate that RE is a disease mediated by Tc2 polarization of the immune response and that its immunohistopathology, natural history, and clinical evolution (chronic, staircase progression) reflect the dual/pleiotropic actions of IL-10, which, depending on the state of activation of the immune system, may be either cytolytic or immunosuppressant.

PMID:
17070736
DOI:
10.1016/j.yebeh.2006.09.006
[Indexed for MEDLINE]
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