Polymorphisms of IL-1β, IL-1Ra, and TNF-α genes: A nested case-control study of their association with risk for stroke

Cvetkovic, Jasmina Trifunovic; Wiklund, Per; Ahmed, Ejaz; Weinehall, Lars; Hallmans, Göran; Lefvert, Ann Kari

doi:10.1016/j.jstrokecerebrovasdis.2004.10.004

Cited by 13 publications

(7 citation statements)

References 40 publications

(34 reference statements)

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“…Accordingly, complement blocking is able to protect animals from the thrombogenic effect of aPL [19]. TLR-4 and TLR-2 in particular provide a crucial first step in triggering the inflammatory response of the innate immunity and have been recently reported to be involved in cell activation mediated by aPL/antib2GPI antibodies in experimental in vitro models [20,21]. More importantly, we found that TLR-4 also plays a role in in vivo animal models of aPL-mediated thrombosis [9].…”

Section: Discussionsupporting

confidence: 50%

Pro-inflammatory genotype as a risk factor for aPL-associated thrombosis: Report of a family with multiple anti-phospholipid positive members

Angelis

Scurati

Raschi

et al. 2009

Journal of Autoimmunity

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Section: Discussionsupporting

confidence: 50%

Pro-inflammatory genotype as a risk factor for aPL-associated thrombosis: Report of a family with multiple anti-phospholipid positive members

Angelis

Scurati

Raschi

et al. 2009

Journal of Autoimmunity

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“…Levels of IL-6 in the serum and in the CSF of acute stroke patients have been reported to correlate with brain infarct volume, stroke severity, and clinical outcome[56,57]. In some studies, genetic variants of IL-1β and IL-1R have been associated with higher risk of stroke[58], although these data were not confirmed in a large prospective study just published[59]. LIF, too, may play a role in postischemic inflammation since increased LIF expression was detected in peri-infarcted regions in an autopsy specimen of acute stroke patients[60] and in a rat model of middle cerebral artery occlusion[61].…”

Section: Inflammation In the Context Of White Matter Disease And In Mmentioning

confidence: 99%

Cytokines and Myelination in the Central Nervous System

Schmitz

Chew²

2008

The Scientific World JOURNAL

118

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Myelin abnormalities that reflect damage to developing and mature brains are often found in neurological diseases with evidence of inflammatory infiltration and microglial activation. Many cytokines are virtually undetectable in the uninflamed central nervous system (CNS), so that their rapid induction and sustained elevation in immune and glial cells contributes to dysregulation of the inflammatory response and neural cell homeostasis. This results in aberrant neural cell development, cytotoxicity, and loss of the primary myelin-producing cells of the CNS, the oligodendrocytes. This article provides an overview of cytokine and chemokine activity in the CNS with relevance to clinical conditions of neonatal and adult demyelinating disease, brain trauma, and mental disorders with observed white matter defects. Experimental models that mimic human disease have been developed in order to study pathogenic and therapeutic mechanisms, but have shown mixed success in clinical application. However, genetically altered animals, and models of CNS inflammation and demyelination, have offered great insight into the complexities of neuroimmune interactions that impact oligodendrocyte function. The intracellular signaling pathways of selected cytokines have also been highlighted to illustrate current knowledge of receptor-mediated events. By learning to interpret the actions of cytokines and by improving methods to target appropriate predictors of disease risk selectively, a more comprehensive understanding of altered immunoregulation will aid in the development of advanced treatment options for patients with inflammatory white matter disorders.

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“…Lee et al [2] presented evidence that TNF-alpha gene polymorphism is associated with the increased susceptibility to ischemic stroke in Korean population. Trifunovic Cvetkovic et al [3] claimed that in Swedish patients the A1A1 genotype of TNFa is associated with risk of stroke. According to Lalouschek et al [4] carriers of the TNF-alpha (308) A allele face an increased risk of stroke only in association with a febrile episode.…”

Section: Introductionmentioning

confidence: 99%

TNFα gene G-308A polymorphism and the risk of ischemic stroke

Wawrzynek

Dobiała²,

Wender³

et al. 2014

Neurologia i Neurochirurgia Polska

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TNFα, a significant immune mediator, may contribute to the initiation and progression of the ischemic stroke. Genetics of TNFα molecule may have an important role in the risk of ischemic stroke. The most interesting aspects of the G-308A polymorphism remain unexplained; there are many discrepancies between the results. Differences in the ethnicity of the studied cohorts may be taken as one of the possibility. Our study material consisted of 101 patients with ischemic stroke, including 30% classified as lacunar stroke. The diagnosis was based on the presence of rapidly developing neurological signs lasting longer then 24h and confirmed by neuroimaging matter. All patients were of Polish Caucasian origin. Randomly selected 100 individuals without any sign of the vascular disease of central nervous system were taken as the control material. The frequency of polymorphism G-308A in TNFα gene was determined as described by Rubattu et al. [11]. The genotype distribution in our material was similar and statistically insignificant between patients and controls. The heterozygotic G/A genotype was detected in 9% of patients and in 15% of control materials, homozygotic A/A was found in 5% of patients and only in one of control and G/G in 87% of patients and in 84% of control individuals. Our results are negative with respect to the impact of 308 TNFα polymorphism on the risk of ischemic stroke in Caucasians living in Poland.

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Polymorphisms of IL-1β, IL-1Ra, and TNF-α genes: A nested case-control study of their association with risk for stroke

Cited by 13 publications

References 40 publications

Pro-inflammatory genotype as a risk factor for aPL-associated thrombosis: Report of a family with multiple anti-phospholipid positive members

Pro-inflammatory genotype as a risk factor for aPL-associated thrombosis: Report of a family with multiple anti-phospholipid positive members

Cytokines and Myelination in the Central Nervous System

TNFα gene G-308A polymorphism and the risk of ischemic stroke

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