Serum Tryptophan, Kynurenine, and Neopterin in Patients with Guillain-Barre-Syndrome (GBS) and Multiple Sclerosis (MS)

Rudzite, Vera; Berzinsh, J.; Grivane, I.; Fuchs, Dietmar; Baier‐Bitterlich, Gabriele; Wächter, Helmut

doi:10.1007/978-1-4613-0381-7_30

Cited by 23 publications

(18 citation statements)

References 16 publications

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“…However, the absence of IDO means that the oligodendrocyte is unable to down regulate the immune response which in turn may render it more vulnerable to immune attack especially in the context of autoimmune diseases affecting the brain. Our in vitro model is applicable to studies of demyelinating diseases such as MS in which KP has been shown to be involved [7,[10][11][12]. However, data concerning the levels of KP metabolites in the serum or CSF from MS patients are controversial.…”

Section: Discussionmentioning

confidence: 96%

Characterization of the kynurenine pathway in human oligodendrocytes

Lim

Smythe

Stocker

et al. 2007

International Congress Series

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Section: Discussionmentioning

confidence: 96%

Characterization of the kynurenine pathway in human oligodendrocytes

Lim

Smythe

Stocker

et al. 2007

International Congress Series

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“…Early studies reported the tryptophan degradation and the activation of the kynurenine pathway in MS in the plasma and cerebrospinal fluid (CSF) of MS patients [109]. Additional studies confirmed these data, describing low concentrations of TRP in serum and CSF from patients with chronic MS [110]. In primary biliary cirrhosis patients, defects in IDO expression have also been observed, which correlated with an increased frequency of a gain‐of‐function SNP within the TGF‐beta promoter region, a molecule known to suppress IDO transcription [111].…”

Section: Intracellular Molecules: Ido and Ahrmentioning

confidence: 89%

Immunoregulatory molecules are master regulators of inflammation during the immune response

Fuente¹,

Cibrián²,

Sánchez-Madrid³

2012

FEBS Letters

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a b s t r a c tThe balance between pro-and anti-inflammatory signalling is critical to maintain the immune homeostasis under physiological conditions as well as for the control of inflammation in different pathological settings. Recent progress in the signalling pathways that control this balance has led to the development of novel therapeutic agents for diseases characterized by alterations in the activation/suppression of the immune response. Different molecules have a key role in the regulation of the immune system, including the receptors PD-1 (Programmed cell Death 1), CTLA-4 (Cytotoxic TLymphocyte Antigen 4) and galectins; or the intracellular enzyme IDO (indoleamine 2,3-dioxygenase). In addition, other molecules as CD69, AhR (Aryl hydrocarbon Receptor), and GADD45 (Growth Arrest and DNA Damage-inducible 45) family members, have emerged as potential targets for the regulation of the activation/suppression balance of immune cells. This review offers a perspective on well-characterized as well as emergent negative immune regulatory molecules in the context of autoimmune inflammatory diseases.

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“…Moreover, an opposing pattern of IDO and IFN-γ mRNA expression was observed in spinal cord and peripheral blood mononuclear cells (PBMCs) through the preclinical, acute and remission phases of EAE [ 12 ], suggesting that IDO and Trp metabolites contribute to the reversible neurological symptoms of MS. Nevertheless, although Trp levels and IDO activity have been repeatedly studied in MS patients [ 14 – 16 ], consistent results have not been obtained, probably due to the variable course of the disease.…”

Section: Introductionmentioning

confidence: 99%

Indoleamine 2,3 Dioxygenase (IDO) Expression and Activity in Relapsing- Remitting Multiple Sclerosis

et al. 2015

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BackgroundInterferon gamma (IFN-γ) production induces the transcription of indoleamine 2,3 dioxygenase (IDO) resulting in the reduction of T-cell activation and proliferation through the depletion of tryptophan and the elicitation of Treg lymphocytes. IDO was shown to be involved in the pathogenesis of autoimmune diseases; we investigated whether changes in IDO gene expression and activity could be indicative of onset of relapse in multiple sclerosis (MS) patients.MethodsIDO and interferon-γ (IFN-γ) gene expression, serum IDO activity (Kynurenine/Tryptophan ratio) and serum neopterin concentration – a protein released by macrophages upon IFN-γ stimulation – were measured in 51 individuals: 36 relapsing remitting (RR)-MS patients (21 in acute phase -AMS, 15 in stable phase -SMS) and 15 healthy controls (HC). PBMCs samples in AMS patients were collected before (BT-AMS) and during glucocorticoids-based therapy (DT-AMS).ResultsIDO expression was increased and IFN-γ was decreased (p<0.001) in BT-AMS compared to SMS patients. Glucocorticoids-induced disease remission resulted in a significant reduction of IDO and IFN-γ gene expression, IDO catalytic activity (p<0.001). Serum neopterin concentration followed the same trend as IDO expression and activity.ConclusionsMeasurement of IDO gene expression and activity in blood could be a useful marker to monitor the clinical course of RR-MS. Therapeutic interventions modulating IDO activity may be beneficial in MS.

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Serum Tryptophan, Kynurenine, and Neopterin in Patients with Guillain-Barre-Syndrome (GBS) and Multiple Sclerosis (MS)

Cited by 23 publications

References 16 publications

Characterization of the kynurenine pathway in human oligodendrocytes

Characterization of the kynurenine pathway in human oligodendrocytes

Immunoregulatory molecules are master regulators of inflammation during the immune response

Indoleamine 2,3 Dioxygenase (IDO) Expression and Activity in Relapsing- Remitting Multiple Sclerosis

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