title: The interleukin 17 system in cortical lesions in focal cortical dysplasias.
abstract: Focal cortical dysplasias (FCDs) are increasingly recognized as important causes of medically intractable epilepsy. To understand the potential role of the interleukin 17 (IL-17) system in the epileptogenesis of FCDs, we studied the expression patterns of the IL-17 system in 15 FCD type Ia (FCDIa), 12 FCD type IIa (FCDIIa), and 12 FCD type IIb (FCDIIb) cortical lesions and compared the results with those in cerebral cortex from 10 control patients. Protein levels of IL-17, IL-17 receptor (IL-17R), and downstream factors of the IL-17 pathway (nuclear factor-κB activator 1 [NFκB; ACT1] and NFκB-p65) were markedly elevated in FCDIa, FCDIIa, and FCDIIb. Moreover, protein levels of IL-17 and IL-17R positively correlated with the frequency of seizures in FCD patients. Immunostaining indicated that IL-17 and IL-17R are highly expressed in neuronal microcolumns, dysmorphic neurons, balloon cells, astrocytes, and vascular endothelial cells. Nuclear factor-κB activator 1 and NFκB-p65 were diffusely expressed in FCDs. In addition, we detected a few IL-17-positive, CD4-positive T lymphocytes in FCDIIa and FCDIIb but not in FCDIa. Taken together, these findings suggest that the overexpression of the IL-17 system and the activation of the IL-17 signal transduction pathway may be involved in the epileptogenicity of cortical lesions in FCDs, thus representing a novel potential target for antiepileptic therapy.
authors: From the Department of Neurosurgery, Xinqiao Hospital, Third Military Medical University, Chongqing, China.
authors: Jiao-Jiang
authors: JJ
authors: He
authors: Song
authors: S
authors: Li
authors: Hai-Feng
authors: HF
authors: Shu
authors: Si-Xun
authors: SX
authors: Yu
authors: Shi-Yong
authors: SY
authors: Liu
authors: Qing
authors: Q
authors: Yin
authors: Hui
authors: H
authors: Yang
mesh_terms: D048868:Adaptor Proteins, Signal Transducing; D000293:Adolescent; D000328:Adult; D002452:Cell Count; D002540:Cerebral Cortex / Q000378:metabolism* / Q000473:pathology; D002648:Child; D002675:Child, Preschool; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006801:Humans; D007223:Infant; D020381:Interleukin-17 / Q000378:metabolism*; D008137:Longitudinal Studies; D054220:Malformations of Cortical Development / Q000145:classification / Q000473:pathology* / Q000601:surgery; D016328:NF-kappa B / Q000378:metabolism; D016900:Neurofilament Proteins / Q000378:metabolism; D053722:Receptors, Interleukin-17 / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology*; D047988:Tumor Necrosis Factor Receptor-Associated Peptides and Proteins / Q000378:metabolism; D055815:Young Adult
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D005904:Glial Fibrillary Acidic Protein; D020381:Interleukin-17; D016328:NF-kappa B; D016900:Neurofilament Proteins; D053722:Receptors, Interleukin-17; C414202:TRAF3IP2 protein, human; D047988:Tumor Necrosis Factor Receptor-Associated Peptides and Proteins; C051774:neurofilament protein H