Journal of Neuroimmunology (J NEUROIMMUNOL )

Publisher: International Society for Neuroimmunology, Elsevier


The Journal of Neuroimmunology affords a forum for the publication of works applying immunologic methodology to the furtherance of the neurological sciences. Studies on all branches of the neurosciences, particularly fundamental and applied neurobiology, neurology, neuropathology, neurochemistry, neurovirology, neuroendocrinology, neuromuscular research, neuropharmacology and psychology, which involve either immunologic methodology (e.g. immunocytochemistry) or fundamental immunology (e.g. antibody and lymphocyte assays), are considered for publication. Works pertaining to multiple sclerosis, AIDS, amyotrophic lateral sclerosis, Guillain Barré Syndrome, myasthenia gravis, and brain tumors form a major focus. The scope of the Journal is broad, covering both research and clinical problems of neuroscientific interest.A major aim of the Journal is to encourage the development of immunologic approaches to analyse in further depth the interactions and specific properties of nervous tissue elements during development and disease.

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    Journal of neuroimmunology
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    • NIH Authors articles will be submitted to PubMed Central after 12 months
    • Publisher last contacted on 18/10/2013
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Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Neurocysticercosis (NCC), a central nervous system (CNS) disease is caused by the larval stage of Taenia solium. The disease is heterogeneous in clinical presentation; some infected individuals develop symptoms and others may remain symptom free. Impaired blood brain barrier allows recruitment of immune cells in the CNS during infection and soluble intercellular adhesion molecule-1 (sICAM-1) plays an important role in the recruitment of immune cells. We studied ICAM-1 K469E polymorphism among symptomatic and asymptomatic NCC patients. The study revealed that individuals with variant (EE) genotype were more susceptible to symptomatic NCC and also had an elevated level of sICAM-1.
    Journal of Neuroimmunology 11/2014;
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    ABSTRACT: The immunomodulatory effects of the IL-27 and IL-33 and the anti-inflammatory effects of ginger have been reported in some studies. The aim was to evaluate the effects of the ginger extract on the expression of IL-27 and IL-33 in a model of experimental autoimmune encephalomyelitis (EAE). In PBS-treated EAE mice the expression of IL-27 P28 was significantly lower whereas the expression of IL-33 was significantly higher than unimmunized control mice. In 200 and 300 mg/kg ginger-treated EAE groups the expression of IL-27 P28 and IL-27 EBI3 was significantly higher whereas the expression of IL-33 was significantly lower than PBS-treated EAE mice. The EAE clinical symptoms and the pathological scores were significantly lower in ginger-treated EAE groups. These results showed that the ginger extract modulates the expression of the IL-27 and IL-33 in the spinal cord of EAE mice and ameliorates the clinical symptoms of disease.
    Journal of Neuroimmunology 11/2014;
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    ABSTRACT: CD4 + T-cells play a key role in the pathogenesis of multiple sclerosis (MS). Altered peptide ligands capable of modulating T-cell autoreactivity are considered a promising strategy for development of antigen-specific therapies for MS. Since peptides are inherently unstable, the current study explored single β-amino acid substitution as a means of stabilizing an epitope of myelin oligodendrocyte glycoprotein. β-amino acid substitution at position 44, the major T-cell receptor contact residue, increased the half-life of active metabolites. Vaccination with one altered peptide, MOG44βF, conferred protection from EAE, decreased T-cell autoreactivity and pro-inflammatory cytokine production. Additional studies using MOG44βF in an oral treatment regimen, administered after EAE induction, also attenuated disease severity. Thus, altered peptides such as those reported here may lead to the development of novel and more specific treatments for MS.
    Journal of Neuroimmunology 10/2014;
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    ABSTRACT: Intravenous immunoglobulin (IVIG) may improve neuroinflammation after traumatic brain injury (TBI). IVIG administration after TBI improved rotarod latencies over the first 7 days (p = 0.039) and water maze latencies over 29–32 days (p = 0.027), decreased F4/80-positive cells at 2 (p = 0.001) and 7 days (p < 0.001), decreased Fluoro-Jade B-positive cells (p = 0.020), increased NeuN-positive cells (p = 0.014), decreased IL-6 production at 4 (p = 0.032) and 24 hours (p = 0.023), and decreased blood–brain barrier breakdown by IgG extravasation (p = 0.001) and brain edema (p = 0.006); however, TNF-α concentration was unchanged. IVIG administration was associated with long-term neurobehavioral and histological improvement through modulation of neuroinflammation and blood–brain barrier permeability in a murine TBI model.
    Journal of Neuroimmunology 09/2014;
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    ABSTRACT: Triggers of brain inflammation in pneumococcal meningitis are unknown. TNF-α and IL-1β were upregulated (real time PCR and in situ hybridization) in neurons and astrocytes time-dependently and maximally in the hippocampus during murine pneumococcal meningitis. Upregulation of TNF-α and IL-1β mRNA in the brain parenchyma was independent of cerebrospinal fluid leukocytosis, pneumococcal pneumolysin and H2O2, but it was potently induced by pneumococcal cell wall (PCW) fragments. Brain TNF-α mRNA was downregulated by a matrix metalloproteinases inhibitor. PCW fragments were located in brain parenchyma. In conclusion, PCW fragments and matrix metalloproteinases trigger cytokine induction in the brain parenchyma during pneumococcal meningitis.
    Journal of Neuroimmunology 09/2014;
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    ABSTRACT: Objective To investigate the association between aquaporin 4 (AQP4) gene polymorphisms and Chinese patients with neuromyelitis optica (NMO). Methods 122 consecutive anti-AQP4 autoantibodies (NMO-IgG) seropositive cases were enrolled for gene sequencing. Furthermore, ten SNPs were selected and genotyped for a case-control association analysis on 208 cases and 204 healthy subjects. Results 14 novel SNPs were identified, while there were no nonsynonymous mutations and their frequency was low. The heterozygous genotype at two 3′ UTR SNPs was significantly higher in cases than controls: the A/T genotype of SNP rs1058424 (54.81% vs. 42.65%, padjusted = 0.024, OR = 1.670, 95% CI = 1.071–2.605) and the C/T genotype of SNP rs3763043 (53.85% vs. 42.65%, padjusted = 0.028, OR = 1.638, 95% CI = 1.054–2.545). Moreover, the 3′ UTR haplotype ATATGGAT may be protective for NMO (7.67% vs. 12.18%, p = 0.042). Conclusions Polymorphisms in the coding region of AQP4 are unlikely to confer NMO susceptibility. However, the 3′ UTR of this gene presents several polymorphic sites that may affect NMO risk in the Chinese.
    Journal of Neuroimmunology 09/2014;
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    ABSTRACT: Immune surveillance of the CNS is critical for preventing infections, however there is no accepted experimental model to assess the risk of infection when utilizing disease-modifying agents. We tested two approved agents for patients with multiple sclerosis (MS), glatiramer acetate and fingolimod, in an experimental model of CNS immune surveillance. C57BL/6 mice were infected with the ME49 strain of the neuroinvasive parasite Toxoplasma gondii (T. gondii) and then treated with GA and fingolimod. Neither treatment affected host survival, however differences were observed in parasite load and in leukocyte numbers in the brains of infected animals. Here we demonstrate that this model could be a useful tool for analyzing immune surveillance.
    Journal of Neuroimmunology 09/2014;
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    ABSTRACT: Background Free copper in Wilson disease (WD) is toxic and may reduce antioxidant, increase oxidative stress marker and thereby cytokine release and excitotoxic injury, but there is paucity of studies in humans. We report oxidative stress markers, cytokines and glutamate in neurologic WD and correlate these with their clinical severity, laboratory findings and extent of Magnetic resonance imaging (MRI) changes. Methods 29 patients with neurologic WD and 9 asymptomatic WD siblings were included and their clinical, treatment history, disease severity, biochemical findings and MRI changes were noted. Glutathione (GSH), total antioxidant capacity (TAC) and malonodialdehyde (MDA) were measured by spectrophotometer, cytokines by cytokine bead array and glutamate by the fluorometer. Results In WD patients, the glutathione (Mean ± SEM, 2.20 ± 0.06Vs2.73 ± 0.04 mg/dl, P < 0.001) and TAC (1.70 ± 0.03 Vs.2.29 ± 0.02 Trolox_Eq_mmol/L, P < 0.001) were reduced, and MDA and glutamate (23.93 ± 0.54Vs. 19.96 ± 0.27 μmol/l; P < 0.001) were increased (4.7 ± 0.11Vs. 3.03 ± 0.52 nmol/ml, P < 0.001) compared to controls. The serum IL6 {median (IQRs), 9.42(10.92) Vs. 5.2(5.34) pg/ml; P = 0.001}, IL8 {12.37(10.92) Vs. 5.63(5.52) pg/ml; P < 0.001}, IL10 {8.33(8.3) Vs. 2.05(1.37) pg/ml; P = 0.001} and TNFα {6.14(8.95) Vs. 3.61(3.58) pg/ml; P < 0.001} were also increased in WD patients compared to controls. These changes were more marked in the neurologic WD compared to asymptomatic WD and in the untreated compared to treated patients. TAC correlated with duration of illness, serum free copper, 24 hour urinary copper and serum ceruloplasmin, and glutamate with MDA, TNFα, ceruloplasmin and 24-hour urinary copper. Conclusions In WD patients, antioxidants are reduced and MDA, cytokines and glutamate are increased which are more marked in symptomatic neurologic WD than asymptomatic patients.
    Journal of Neuroimmunology 09/2014;
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    ABSTRACT: In the present study, we investigated the therapeutic benefit of Cornel iridoid glycoside (CIG), main component extracted from Cornus officinalis, in experimental autoimmune encephalomyelitis (EAE) rats. CIG was intragastrically administered daily after EAE initiation for 20 days and reduced disease severity, incidence, disease onset and ongoing paralysis. Histopathological staining showed that CIG could reduce T cell entry to the central nervous system and microglia activation, increased brain-derived neurotrophic factor (BDNF) expression and mature oligodendrocytes, and decreased oligodendrocyte progenitor cells (OPCs). Also, CIG treatment inhibited brain JAK/STAT1/3 and reduced proinflammatory cytokines. CIG might be a novel potential therapeutic agent for multiple sclerosis (MS).
    Journal of Neuroimmunology 09/2014;
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    ABSTRACT: We previously demonstrated that interferon β (IFN-β)-secreting mesenchymal stem cells (MSCs-IFN-β) strongly reduced the clinical severity of experimental autoimmune encephalomyelitis (EAE), compared with MSCs alone. Recently, minocycline ameliorates the clinical severity of multiple sclerosis (MS). Herein, we evaluated the effects of combined treatment of MSCs-IFN-β and minocycline on EAE mice. The combined treatment significantly alleviated the clinical severity mainly by maintaining the integrity of blood-spinal cord barrier, in a manner likely involving inhibition of microvascular disruption, matrix metalloproteinases, neuroinflammation, and enhancement of immunomodulatory effects. Therefore, this combined treatment has the potential to improve the functional recovery of patients with MS.
    Journal of Neuroimmunology 09/2014;
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    ABSTRACT: Treatment of central nervous system (CNS) autoimmune disorders frequently involves the reduction, or depletion of immune-competent cells. Alternatively, immune cells are being sequestered away from the target organ by interfering with their movement from secondary lymphoid organs, or their migration into tissues. These therapeutic strategies have been successful in multiple sclerosis (MS), the most prevalent autoimmune inflammatory disorder of the CNS. However, many of the agents that are currently approved or in clinical development also have severe potential adverse effects that stem from the very mechanisms that mediate their beneficial effects by interfering with CNS immune surveillance. This review will outline the main cellular components of the innate and adaptive immune system that participate in host defense and maintain immune surveillance of the CNS. Their pathogenic role in MS and its animal model experimental autoimmune encephalomyelitis (EAE) is also discussed. Furthermore, an experimental model is introduced that may assist in evaluating the effect of therapeutic interventions on leukocyte homeostasis and function within the CNS. This model or similar models may become a useful tool in the repertoire of pre-clinical tests of pharmacological agents to better explore their potential for adverse events.
    Journal of Neuroimmunology 08/2014;
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    ABSTRACT: Correlation between gadolinium-enhancing [Gd(+)] lesions on MRI and expression of CD6 molecule and a group of chemokine receptors on peripheral blood (PB) and cerebrospinal fluid (CSF) immune cells was measured in multiple sclerosis (MS) patients. Twenty remitting relapsing MS patients with (n = 10) and without (n = 10) Gd(+) lesions entered the study. mRNA and surface expression of CD6 and CCR1, CCR2, CCR3 and CCR5 was measured by immunostaining and flow cytometry. Expression of mRNA and surface staining for CD6 in PB T lymphocytes was increased in Gd(+) compared to Gd(-) patients (p < 0,01; p < 0,05, respectively). CD6 mRNA correlated with the number and size of Gd(+) lesions (r = 0,67, and r = 0,65 respectively). mRNA and surface expression for CCR1, CCR2, and CCR3 in PB cells was lower in Gd(+) compared to Gd(-) MS patients (p < 0,05, p < 0,05). The frequency of cells co-expressing CD6 with CCR1 and CCR5 was low in PB T lymphocytes and high in CSF (p < 0,05, p < 0,05). These results suggest that Gd(+) correlates with increased expression of CD6 and decresed expression of chemokine receptors on PB T lymphocytes. Co-expression of CD6 with CCR1 and CCR5 predisposes cells for transmigration into CSF.
    Journal of Neuroimmunology 08/2014;
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    ABSTRACT: Background : Multiple sclerosis (MS) is a CNS inflammatory demyelinating disorder. T helper 1 (Th1) and T helper 17 (Th17) cells are important in MS immunopathogenesis. Level of endothelin-1 (ET-1), a potent vasoconstrictor, is increased in sera of MS patients. We studied the role of ET-1 in experimental allergic encephalomyelitis (EAE), a MS animal model. Methods : EAE is induced in transgenic mice overexpressing endothelial ET-1 (TET-1), transgenic mice overexpressing astrocytic ET-1 (GET-1) and non-transgenic (NTg) mice by immunization with myelin oligodendrocyte glycoprotein (MOG)35–55 peptide. EAE scores, spinal cord histology, serum proinflammatory cytokines levels, and proinflammatory cytokines production from splenocytes of ET-1 transgenic and NTg mice with EAE were studied. Results : ET-1 transgenic mice developed more severe EAE than NTg with increased inflammation and demyelination in spinal cord. The mean maximum EAE scores for GET-1, TET-1 and NTg mice with EAE were 4.84, 4.31 and 4.05 respectively (p < 0.05). Serum levels of IL-6, IL-17A, IFN-γ and TNF-α were higher in ET-1 transgenic than NTg mice with EAE (p < 0.05) while serum IL-4 levels were similar. mRNA levels of IL-6, IL-17A, IFN-γ and TNF-α from cultured splenocytes were higher in ET-1-transgenic than NTg mice with EAE (p < 0.05) while IL-4 mRNA levels were similar. Consistently, levels of IL-6, IL-17A, IFN-γ and TNF-α in culture media of splenocytes were higher in ET-1 transgenic than NTg mice with EAE (p < 0.05) while IL-4 levels were similar. Conclusions : Mice with endothelial or astrocytic ET-1 overexpression developed more severe EAE with increased splenic lymphocytes production of Th1 and Th17 proinflammatory cytokines.
    Journal of Neuroimmunology 08/2014;