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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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Department of Neurology and Comprehensive Epilepsy Center, University of Kansas Medical Center, Kansas City, KS, USA.


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.

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