T-Cell Subsets and Interleukin-6 Response in Rasmussen’s Encephalitis

Tekgül, Hasan; Polat, Muzaffer; Kitiş, Ömer; Serdaroğlu, Gül; Tosun, Ayşe; Terlemez, Semiha; Kütükçüler, Necil; Erşahin, Yusuf; Gökben, Sarenur

doi:10.1016/j.pediatrneurol.2005.01.007

Cited by 10 publications

(7 citation statements)

References 21 publications

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“…Although reports about the pathogenic role of cytokines in RS are few (Tekgul et al, 2005; Ganor et al., 2004b), cytokines are highlighted as inflammatory mediators that alter neuronal excitability and affect cell survival (Vezzani et al, 2008). We studied surface markers of T cells, cytokines, and Granzyme B in CSF samples from 27 patients with RS, and evaluated their evolutional changes to reveal their roles in immunopathogenesis, and examine their possible contribution to the diagnosis.…”

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confidence: 99%

A substantial number of Rasmussen syndrome patients have increased IgG, CD4⁺ T cells, TNFα, and Granzyme B in CSF

et al. 2009

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Summary Purpose: We studied the immunologic molecules in cerebrospinal fluid (CSF) and discussed their evolutional changes in pediatric patients with Rasmussen syndrome (RS). Methods: CSF samples collected from 27 patients with RS (average onset age, 7.5 ± 5.6 years) were studied. Cell count, protein, glucose, albumin, chloride, and immunoglobulin G (IgG) levels were measured by conventional methods. Surface markers of lymphocytes in CSF were examined by a cell sorter. Granzyme B, interferon γ (IFNγ), interleukin 4 (IL‐4), tumor necrosis factor α (TNFα), and IL‐12 in CSF were quantitated by enzyme‐linked immunosorbent assay (ELISA). Autoantibodies against GluR ε2 (NR2B) were examined by immunoblot. Results: The data of the first CSF examination showed that IgG levels (Mann‐Whitney U test, p < 0.01), CD4+ T cells (p = 0.02), TNFα levels (p < 0.01), and Granzyme B levels (p < 0.01) were elevated compared with disease controls. White blood cell count, IFNγ level, IL‐12 level, and Granzyme B level were elevated, especially in the early stage of disease. CD4+ T cells, CD8+ cells, CD3+ T cells, IgG levels, and TNFα levels were elevated at all stages of disease evolution. Protein levels and albumin levels were elevated in the progressed stage. Autoantibodies against GluR ε2 (NR2B) (IgG) were found in 50% of patients in the early stage, and the positive rate was low at the progressed stage. Discussion: The present findings suggest that complex pathophysiologic mechanisms involving CD4+ T cells and CD8+ T cells change evolutionally during the progression of RS. A crucial cytotoxic process occurs in the early stage, and declines in the progressed stage.

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confidence: 99%

A substantial number of Rasmussen syndrome patients have increased IgG, CD4⁺ T cells, TNFα, and Granzyme B in CSF

et al. 2009

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“…7% of these infiltrating CD8 + cells are granzyme B-positive, and vesicles were often found positioned adjacent to MHC class I-expressing neurons and astrocytes with their granules polarized toward their target(s), suggesting a cytotoxic T cell-mediated disease course of RE (112). In addition to increased levels of granzyme B at initial stages of disease (113), Tekgul et al revealed raised concentrations of the cytokine IL-6 in the CSF of RE patients compared to controls (114). A correlation was then established between the magnitude of neuronal death and inflammation with the level of IL-6 in the CNS of these patients, based on magnetic resonance spectroscopy (114).…”

Section: T Cell-mediated Cns Diseasesmentioning

confidence: 99%

“…In addition to increased levels of granzyme B at initial stages of disease (113), Tekgul et al revealed raised concentrations of the cytokine IL-6 in the CSF of RE patients compared to controls (114). A correlation was then established between the magnitude of neuronal death and inflammation with the level of IL-6 in the CNS of these patients, based on magnetic resonance spectroscopy (114). The overproduction of IL-6 has been attributed to overstimulation of TNF-α early in disease (113).…”

Section: T Cell-mediated Cns Diseasesmentioning

confidence: 99%

Expanding Role of T Cells in Human Autoimmune Diseases of the Central Nervous System

et al. 2017

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It is being increasingly recognized that a dysregulation of the immune system plays a vital role in neurological disorders and shapes the treatment of the disease. Aberrant T cell responses, in particular, are key in driving autoimmunity and have been traditionally associated with multiple sclerosis. Yet, it is evident that there are other neurological diseases in which autoreactive T cells have an active role in pathogenesis. In this review, we report on the recent progress in profiling and assessing the functionality of autoreactive T cells in central nervous system (CNS) autoimmune disorders that are currently postulated to be primarily T cell driven. We also explore the autoreactive T cell response in a recently emerging group of syndromes characterized by autoantibodies against neuronal cell-surface proteins. Common methodology implemented in T cell biology is further considered as it is an important determinant in their detection and characterization. An improved understanding of the contribution of autoreactive T cells expands our knowledge of the autoimmune response in CNS disorders and can offer novel methods of therapeutic intervention.

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“…14 The pathological examination of 45 hemispherectomies revealed the presence of inflammatory cells ranging from T-cell infiltration and neuroglial reactions to extensive neuronal death. 15 Furthermore, Bien et al 16 found evidence of T-cell-mediated cytotoxicity in specimens of 11 patients. This evidence suggests a role for inflammatory components in the pathogenesis and ongoing progression of Rasmussen encephalitis.…”

Section: Inflammatory Mediators In Epilepsymentioning

confidence: 99%

Targeting inflammation as a therapeutic strategy for drug-resistant epilepsies

Vitaliti

Pavone

Mahmood

et al. 2014

Human Vaccines & Immunotherapeutics

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An increasing body of literature data suggests that inflammation, and in particular neuroinflammation, is involved in the pathophysiology of particular forms of epilepsy and convulsive disorders. Animal models have been used to identify inflammatory triggers in epileptogenesis and inflammation has recently been shown to enhance seizures. For example, pharmacological blockade of the IL-1beta/IL-1 receptor type 1 axis during epileptogenesis has been demonstrated to provide neuroprotection in temporal lobe epilepsy. Furthermore, experimental models have suggested that neural damage and the onset of spontaneous recurrent seizures are modulated via complex interactions between innate and adaptive immunity. However, it has also been suggested that inflammation can occur as a result of epilepsy, since animal models have also shown that seizure activity can induce neuroinflammation, and that recurrent seizures maintain chronic inflammation, thereby perpetuating seizures. On the basis of these observations, it has been suggested that immune-mediated therapeutic strategies may be beneficial for treating some drug resistant epilepsies with an underlying demonstrable inflammatory process. Although the potential mechanisms of immunotherapeutic strategies in drug-resistant seizures have been extensively discussed, evidence on the efficacy of such therapy is limited. However, recent research efforts have been directed toward utilizing the potential therapeutic benefits of anti-inflammatory agents in neurological disease and these are now considered prime candidates in the ongoing search for novel anti-epileptic drugs. The objective of our review is to highlight the immunological features of the pathogenesis of seizures and to analyze possible immunotherapeutic approaches for drug resistant epilepsies that can alter the immune-mediated pathogenesis.

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T-Cell Subsets and Interleukin-6 Response in Rasmussen’s Encephalitis

Cited by 10 publications

References 21 publications

A substantial number of Rasmussen syndrome patients have increased IgG, CD4⁺ T cells, TNFα, and Granzyme B in CSF

A substantial number of Rasmussen syndrome patients have increased IgG, CD4⁺ T cells, TNFα, and Granzyme B in CSF

Expanding Role of T Cells in Human Autoimmune Diseases of the Central Nervous System

Targeting inflammation as a therapeutic strategy for drug-resistant epilepsies

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T-Cell Subsets and Interleukin-6 Response in Rasmussen’s Encephalitis

Cited by 10 publications

References 21 publications

A substantial number of Rasmussen syndrome patients have increased IgG, CD4+ T cells, TNFα, and Granzyme B in CSF

A substantial number of Rasmussen syndrome patients have increased IgG, CD4+ T cells, TNFα, and Granzyme B in CSF

Expanding Role of T Cells in Human Autoimmune Diseases of the Central Nervous System

Targeting inflammation as a therapeutic strategy for drug-resistant epilepsies

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Product

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A substantial number of Rasmussen syndrome patients have increased IgG, CD4⁺ T cells, TNFα, and Granzyme B in CSF

A substantial number of Rasmussen syndrome patients have increased IgG, CD4⁺ T cells, TNFα, and Granzyme B in CSF