Serum cytokine levels are altered in patients with West syndrome

Zs, Liu; Wang, Qinwen; Wang, Fanglin; Yang, Lizhi

doi:10.1016/s0387-7604(01)00313-8

Cited by 43 publications

(39 citation statements)

References 15 publications

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“…Similarly, the IL receptor antagonist (IL-1ra) seems to be decreased during the active stage of IS [107] and increased after the resolution of symptoms of IS [108]. IL-2, interferon-α, and tumor necrosis factor-α were also reported to be increased in the serum of patients with IS [109]. These findings were equally relevant for both patients with IS of structural/metabolic or unknown etiology [108,109].…”

Section: Neuroinflammatory Mechanismsmentioning

confidence: 90%

“…IL-2, interferon-α, and tumor necrosis factor-α were also reported to be increased in the serum of patients with IS [109]. These findings were equally relevant for both patients with IS of structural/metabolic or unknown etiology [108,109]. However, cerebrospinal fluid (CSF) concentrations of the classical proinflammatory IL-6 were significantly lower in patients with IS than in patients with generalized tonic-clonic seizures due to infection or trauma [110].…”

Section: Neuroinflammatory Mechanismsmentioning

confidence: 93%

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Mechanisms of Epileptogenesis in Pediatric Epileptic Syndromes: Rasmussen Encephalitis, Infantile Spasms, and Febrile Infection-related Epilepsy Syndrome (FIRES)

2014

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The mechanisms of epileptogenesis in pediatric epileptic syndromes are diverse, and may involve disturbances of neurodevelopmental trajectories, synaptic homeostasis, and cortical connectivity, which may occur during brain development, early infancy, or childhood. Although genetic or structural/metabolic factors are frequently associated with agespecific epileptic syndromes, such as infantile spasms and West syndrome, other syndromes may be determined by the effect of immunopathogenic mechanisms or energy-dependent processes in response to environmental challenges, such as infections or fever in normally-developed children during early or late childhood. Immune-mediated mechanisms have been suggested in selected pediatric epileptic syndromes in which acute and rapidly progressive encephalopathies preceded by fever and/or infections, such as febrile infection-related epilepsy syndrome, or in chronic progressive encephalopathies, such as Rasmussen encephalitis. A definite involvement of adaptive and innate immune mechanisms driven by cytotoxic CD8 +

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Section: Neuroinflammatory Mechanismsmentioning

confidence: 90%

Section: Neuroinflammatory Mechanismsmentioning

confidence: 93%

Mechanisms of Epileptogenesis in Pediatric Epileptic Syndromes: Rasmussen Encephalitis, Infantile Spasms, and Febrile Infection-related Epilepsy Syndrome (FIRES)

2014

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“…Plasma and CSF levels of cytokines have been studied in patients with WS resulting in inconclusive results. [24][25][26] The mechanisms for WS and the role of immune and inflammatory processes might be elucidated by understanding the mechanisms by which ACTH and steroids suppress WS. These mechanisms are likely multiple and include direct effects on neuronal excitability, suppression of the levels of endogenous proconvulsant molecules such as corticotropin-releasing hormone and antiinflammatory effects.…”

Section: Gad Antibodiesmentioning

confidence: 99%

Epilepsy and Autoimmunity

Çoban¹,

Eki̇zoğlu²,

Tüzün³

2013

Epilepsi

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SummaryEpilepsy may present as a symptom of many neurological disorders and often an etiological factor cannot be identified. There is some evidence that immune mechanisms might play a role in the pathogenesis of certain epileptic syndromes. The evidence in support of this idea includes apparent association of seizures with certain autoimmune diseases, numerous reports of the detection of theoretically relevant serum autoantibodies, an acute or subacute onset of the seizures, a rapidly progressive course, and a favorable response to immunotherapy.In this article, we summarize (i) epilepsies where clinical and biologic data strongly support the pathogenic role of autoantibodies. (ii) epilepsies where immune-mediated inflammation occurs, but the full pathogenic cascade is either not clear or only strongly hypothesized and (iii) autoimmune diseases associated with seizures or epilepsy.Key words: Autoantibodies; autoimmunity; epilepsy. ÖzetEpilepsi birçok nörolojik hastalığın belirtisi olarak ortaya çıkabilir ve sıklıkla etiyolojik faktör tespit edilemez. İmmün mekanizmaların belirli epileptik sendromların patogenezinde rol oynayabileceğine dair bazı kanıtlar vardır. Belli otoimmün hastalıklar ile nöbetlerin açık bir şekilde ilişkili olması, teorik olarak uygun serum otoantikorlarının saptandığı çok sayıda bildirinin olması, akut ya da subakut başlangıçlı nöbetler, hızlı ilerleyici bir seyir ve immünoterapiye olumlu cevap alınması bu fikri destekleyen kanıtlardır. Bu makale, (i) epilepsilerin klinik ve biyolojik verilerinin otoantikorların patolojik rolünü kuvvetli bir şekilde desteklediğini (ii) epilepsilerde immün aracılı inflamasyonun oluştuğunu ancak tam patojenik kaskadın net olmadığını ya da sadece kuvvetli bir hipotez olduğunu ve (iii) epilepsi ya da nöbetlerle ilişkili otoimmün hastalıkları özetlemektedir.

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“…Were associated to WS multiple pathologies in Central Nervous System (CNS), such as structural anomalies, prematurity, phakomatoses, and CNS infections. But despite the multiple underlying factors, there are common clinical and electroencephalographic (EEG) patterns of WS that indicate a "final common pathway" for the pathophysiology of WS 1 . Ten to 20% of cases are considered idiopathic, with no evidence of brain lesions.…”

mentioning

confidence: 99%

“…According to the present knowledge about WS, spasms seem to involve subcortical structures, and hypsarrhythmia affects cortical areas, causing psychomotor deterioration 2 . Even though the pathogenesis is still unclear, a disturbance of immune function in the brain has been considered a possible factor 1 …”

mentioning

confidence: 99%

Immunologic aspects of West syndrome and evidence of plasma inhibitory effects on T cell function

Montelli

Soares

Peraçoli

2003

Arq. Neuro-Psiquiatr.

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-Study objective: : :: : The purpose of this study was to assess the extent of immune dysfunction in a well-defined group of epileptic patients: children with diagnosis of West syndrome (WS) or with transitions to another age-related EEG patterns, the multifocal independent spikes (MIS), and the slow spike-wave complexes (Lennox-Gastaut syndrome -LGS). Thus, WS was studied at different points of the natural evolutive history of the disease. Method: A group of 50 patients (33 with WS, 10 with LGS and 7 with MIS) and 20 age-matched healthy controls were submitted to enumeration of T lymphocyte subsets: CD1, CD3, CD4, CD8, CD4/CD8 ratio and lymphocyte proliferation assay to phytohaemagglutinin (PHA), in the presence of autologous and AB, homologous plasma. Dinitrochlorobenzene (DNCB) skin test sensitization was performed only in patients. Determinations of IgG, IgA, and IgM serum levels were compared to standard values for Brazilian population in different age ranges. Results: Sensitization to DNCB showed absent or low skin reactions in 76% of the patients. High levels of IgG (45.7%) and IgM (61.4%), and lower levels of IgA (23.9%) were detected in the serum of the patients. Enumeration of lymphocyte subsets in peripheral blood showed: low CD3+ (p<0.05), low CD4+ (p<0.05), high CD8+ (p<0.01) and low CD4+ / CD8+ ratio (p<0.001). The proportion of CD1+ cells in the control group was less than 3%, while ranged between 6 and 11 % in 18% of the patients. The in vitro PHA-induced T cell proliferation showed significantly low blastogenic indices only when patients , cells were cultured in presence of their own plasma. No differences in blastogenic indices were observed when the cells of patients and controls were cultured with human AB plasma. Conclusion: The immunodeficiency in WS was mainly characterized by anergy, impaired cell-mediated immunity, altered levels of immunoglobulins, presence of immature thymocytes in peripheral blood and functional impairment of T lymphocytes induced by plasma inhibitory factors.KEY WORDS: dinitrochlorobenzene, West syndrome, Lennox-Gastaut syndrome, multifocal-independent spike syndrome, T-lymphocytes subsets, immunoglobulins, proliferation assay, T cells, CD1, CD3, CD4, CD8.Aspectos imunológicos da síndrome de W Aspectos imunológicos da síndrome de W Aspectos imunológicos da síndrome de W Aspectos imunológicos da síndrome de W Aspectos imunológicos da síndrome de West e evidência de efeitos inibitórios do plasma sobre a função est e evidência de efeitos inibitórios do plasma sobre a função est e evidência de efeitos inibitórios do plasma sobre a função est e evidência de efeitos inibitórios do plasma sobre a função est e evidência de efeitos inibitórios do plasma sobre a função de células T de células T de células T de células T de células T RESUMO -Objetivo: O objetivo deste estudo foi determinar o perfil da deficiência imune em um grupo bem definido de epilepsia: crianças com síndrome de West (SW) e seus padrões EEG de evolução, idade-dependentes, como os complexos onda-agud...

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Serum cytokine levels are altered in patients with West syndrome

Cited by 43 publications

References 15 publications

Mechanisms of Epileptogenesis in Pediatric Epileptic Syndromes: Rasmussen Encephalitis, Infantile Spasms, and Febrile Infection-related Epilepsy Syndrome (FIRES)

Mechanisms of Epileptogenesis in Pediatric Epileptic Syndromes: Rasmussen Encephalitis, Infantile Spasms, and Febrile Infection-related Epilepsy Syndrome (FIRES)

Epilepsy and Autoimmunity

Immunologic aspects of West syndrome and evidence of plasma inhibitory effects on T cell function

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