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 website
  • Other titles
    Journal of neuroimmunology
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  • Document type
    Journal / Magazine / Newspaper, Internet Resource

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    • Articles in some journals can be made Open Access on payment of additional charge
    • 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: Aquaporin-4 (AQP-4) antibody-positive longitudinally extensive transverse myelitis (LETM) is referred to as a neuromyelitis optica (NMO) spectrum disorder. We conducted an exploratory investigation of correlations between AQP-4 antibody serum levels, as determined by a fluorescent immunoprecipitation assay, and clinical characteristics in LETM. Expanded Disability Status Scores (EDSS) scores and number of segments of spinal cord involved were positively correlated to AQP-4 antibody levels. However, serum AQP-4 antibody levels were not correlated with the time to next attack or the conversion time of LETM to NMO, although seropositive LETM patients demonstrated a high conversion rate to NMO (78.1%).
    Journal of Neuroimmunology 01/2015; 278.
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    ABSTRACT: Neuroinflammation can damage the brain and plays a critical role in the pathophysiology of epilepsy. Tissue inhibitor of metalloproteinase 4 (TIMP4) is an inflammation-induced apoptosis and matrix turnover factor involved in several neuronal disorders and inflammatory diseases. Evidence has shown linkage disequilibrium between rs3755724 (–55C/T) of this gene with synapsin 2 (SYN2) rs3773364 and peroxisome proliferator-activated G receptor (PPARG) rs2920502 loci, which contribute to epilepsy in Caucasians. The aim of this study was to examine the association of these loci alone or their haplotypes with the risk of epilepsy in the Malaysian population. Genomic DNA of 1241 Malaysian Chinese, Indian, and Malay subjects (670 patients with epilepsy and 571 healthy individuals) was genotyped for the candidate loci by using the Sequenom MassArray method. Allele and genotype association of rs3755724 with susceptibility to epilepsy was significant in the Malaysian Chinese with focal epilepsy under codominant and dominant models (C vs. T: 1.5 (1.1–2.0), p = 0.02; CT vs. TT: 1.8 (1.2–2.8), p = 0.007 and 1.8 (1.2–2.7), p = 0.006, respectively). The T allele and the TT genotype were more common in patients than in controls. No significant association was found between rs2920502 and rs3773364–rs3755724–rs2920502 haplotypes for susceptibility to epilepsy in each ethnicity. This study provides evidence that the promoter TIMP4 rs3755724 is a new focal epilepsy susceptibility variant that is plausibly involved in inflammation-induced seizures in Malaysian Chinese.
    Journal of Neuroimmunology 12/2014;
  • Journal of Neuroimmunology 12/2014;
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    ABSTRACT: The study was undertaken considering age-related changes in susceptibility to experimental autoimmune encephalomyelitis (EAE) and a putative role of spleen in pathogenesis of this disease. The phenotypic and functional characteristics of T splenocytes were examined in young (3-month-old), middle-aged (8-month-old) and aged (26-month-old) Dark Agouti rats immunized for EAE with rat spinal cord in complete Freund's adjuvant. The rat susceptibility to EAE induction, as well as the number of activated CD4 + CD134 + lymphocytes retrieved from their spinal cords progressively decreased with aging. To the contrary, in rats immunized for EAE the number of activated CD4 + splenocytes, i.e. CD4 + CD134 +, CD4 + CD25 + FoxP3– and CD4 + CD40L + cells, progressively increased with aging. This was associated with age-related increase in (i) CD4 + splenocyte surface expression of CD44, the molecule suggested to be involved in limiting emigration of encephalitogenic CD4 + cells from spleen into blood and (ii) frequency of regulatory T cells, including CD4 + CD25 + FoxP3 + cells, which are also shown to control encephalitogenic cell migration from spleen into the central nervous system. In favor of expansion of T-regulatory cell pool in aged rats was the greater concentration of IL-10 in unstimulated, Concanavalin A (ConA)- and myelin basic protein (MBP)-stimulated splenocyte cultures from aged rats compared with the corresponding cultures from young ones. Consistent with the age-related increase in the expression of CD44, which is shown to favor Th1 effector cell survival by interfering with CD95-mediated signaling, the frequency of apoptotic cells among CD4 + splenocytes, despite the greater frequency of CD95 + cells, was diminished in splenocyte cultures from aged compared with young rats. In addition, in control, as well as in ConA- and MBP-stimulated splenocyte cultures from aged rats, despite of impaired CD4 + cell proliferation, IFN-γ concentrations were greater than in corresponding cultures from young rats. This most likely reflected increased abundance of IFN-γ-producing cells in splenocyte cultures from aged compared with young rats. The diminished CD4 + cell proliferation in response to ConA and MBP in splenocyte cultures from aged compared with young rats could be, at least partly, associated with an enhanced splenic expression of iNOS mRNA in aged rats. Thus, the study suggests that age-associated changes leading to entrapping of activated CD4 + cells in the spleen could contribute to the restriction in development of EAE in aged rats.
    Journal of Neuroimmunology 12/2014;
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    ABSTRACT: The mechanisms by which neurons respond to inflammatory mediators such as interferons (IFNs) remain largely undefined. We previously showed that the activation and nuclear localization of the core IFN signaling molecule, Stat1, are muted and delayed in primary mouse hippocampal neurons treated with IFN gamma as compared to control mouse embryonic fibroblasts (MEF). Here, we show that the kinetics of Stat1 and Stat2 activation following type I IFN exposure are also unique in neurons, affecting gene expression and neuronal response. Specifically, despite lower basal expression of many IFN stimulated genes in neurons, basal expression of the type I IFN themselves is significantly higher in primary hippocampal neurons compared to MEF. Elevated homeostatic IFN in neurons is critical and sufficient for early control of viral infection. These data provide further evidence that neurons exploit unique signaling responses to IFNs, and define an important contribution of homeostatic IFN within the CNS. Such differences are likely critical for the ability of neurons to survive a viral challenge.
    Journal of Neuroimmunology 12/2014;
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    ABSTRACT: During postnatal development, microglia, CNS resident innate immune cells, are essential for synaptic pruning, neuronal apoptosis and remodeling. During this period microglia undergo morphological and phenotypic transformations; however, little is known about how microglial number and density is regulated during postnatal CNS development. We found that after an initial increase during the first 14 postnatal days, microglial numbers in mouse brain began declining in the third postnatal week and were reduced by 50% by 6weeks of age; these "adult" levels were maintained until at least 9months of age. Microglial CD11b levels increased, whereas CD45 and ER-MP58 declined between P10 and adulthood, consistent with a maturing microglial phenotype. Our data indicate that both increased microglial apoptosis and a decreased proliferative capacity contribute to the developmental reduction in microglial numbers. We found no correlation between developmental reductions in microglial numbers and brain mRNA levels of Cd200, Cx3Cl1, M-Csf or Il-34. We tested the ability of M-Csf-overexpression, a key growth factor promoting microglial proliferation and survival, to prevent microglial loss in the third postnatal week. Mice overexpressing M-Csf in astrocytes had higher numbers of microglia at all ages tested. However, the developmental decline in microglial numbers still occurred, suggesting that chronically elevated M-CSF is unable to overcome the developmental decrease in microglial numbers. Whereas the identity of the factor(s) regulating microglial number and density during development remains to be determined, it is likely that microglia respond to a "maturation" signal since the reduction in microglial numbers coincides with CNS maturation. Copyright © 2014 Elsevier B.V. All rights reserved.
    Journal of Neuroimmunology 11/2014;
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    ABSTRACT: Regulatory T cells (Tregs) mediate immune tolerance to self and depend on IL-2 for homeostasis. Treg deficiency, dysfunction, and instability are implicated in the pathogenesis of numerous autoimmune diseases. There is considerable interest in therapeutic modulation of the IL-2 pathway to treat autoimmunity, facilitate transplantation tolerance, or potentiate tumor immunotherapy. Daclizumab is a humanized mAb that binds the IL-2 receptor α subunit (IL-2Rα or CD25) and prevents IL-2 binding. In this study, we investigated the effect of daclizumab-mediated CD25 blockade on Treg homeostasis in patients with relapsing-remitting multiple sclerosis. We report that daclizumab therapy caused an ∼50% decrease in Tregs over a 52-wk period. Remaining FOXP3(+) cells retained a demethylated Treg-specific demethylated region in the FOXP3 promoter, maintained active cell cycling, and had minimal production of IL-2, IFN-γ, and IL-17. In the presence of daclizumab, IL-2 serum concentrations increased and IL-2Rβγ signaling induced STAT5 phosphorylation and sustained FOXP3 expression. Treg declines were not associated with daclizumab-related clinical benefit or cutaneous adverse events. These results demonstrate that Treg phenotype and lineage stability can be maintained in the face of CD25 blockade. Copyright © 2014 by The American Association of Immunologists, Inc.
    Journal of Neuroimmunology 11/2014;
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    ABSTRACT: The sympathetic nervous system regulates many immune functions and modulates the anti-tumor immune defense response, too. Therefore, we studied the effect of 6-hydroxydopamine induced sympathectomy on selected hematological parameters and inflammatory markers in rats with Yoshida AH130 ascites hepatoma. We found that chemically sympathectomized tumor-bearing rats had significantly increased neutrophil-to-lymphocyte ratio, leukocyte-to-lymphocyte ratio, and plasma levels of tumor necrosis factor alpha. Although our findings showed that sympathetic denervation in tumor-bearing rats led to increased neutrophil-to-lymphocyte ratio, that is an indicator of the disease progression, we found no significant changes in tumor growth and survival of sympathectomized tumor-bearing rats. Copyright © 2014 Elsevier B.V. All rights reserved.
    Journal of Neuroimmunology 11/2014;
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    ABSTRACT: Interest is rising for auto-immune contribution in neuro-psychiatry. We evaluated the auto-antibodies against dopamine transporter (DAT aAbs) in 61 children (46 ADHD who met DSM-IV-TR criteria, 15 healthy controls). ADHD patients were assigned, according to severity, either to a non-pharmacological therapy (NPT, N=32) or to a pharmacological treatment (PT, N=14) with methylphenidate (MPH). In ADHD children, blood samples were withdrawn twice, at recruitment (T0 basal) and after 6weeks (T1); following 16 excluded subjects, DAT genotype was characterized (9-repeat or 10-repeat alleles; N=15 each). After 18months of NPT or PT, some patients (carrying at least one 9-repeat allele) were blood sampled again (T2), for comparison with healthy controls (final n=8) RESULTS: Compared to NPT, basal DAT aAbs titers were higher within most severe patients (then assigned to PT), specifically if carrying a DAT 10/10 genotype. DAT aAbs levels of NPT group resulted highly correlated with distinct subscales of Conners' Parent/Teacher Scales (Rs>0.34), especially within DAT 10/10 genotype (Rs>0.53). While T1 titers were elevated over T0 baseline for NPT children, such an increase was not observed in PT patients carrying at least one 9-repeat allele, who also showed behavioral response to subchronic MPH. After 12-24 months of MPH exposure, DAT aAbs titers in PT subjects were comparable to those of healthy controls, while titers remained significantly elevated in NPT patients. Data warrant further research on serum DAT aAbs, which could be used to confirm ADHD diagnosis and/or to monitor therapeutic efficacy of MPH. Copyright © 2014 Elsevier B.V. All rights reserved.
    Journal of Neuroimmunology 11/2014;
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    ABSTRACT: The influence of the innate immunity on GBM pathology remains unclear.•We investigated complement activation and progression in glial tumor patients.•Key-proteins of the alternative and classical pathways were decreased in GBM patients.•MBL deficiency was less frequent among GBM patients compared to controls.•Lower frequency of MBL deficiency may suggest a protective effect on tumor initiation.
    Journal of Neuroimmunology 11/2014;
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    ABSTRACT: While follicular helper T (Tfh) cells have been shown to be involved in many autoimmune diseases, the association of Tfh cells with the disease activity of neuromyelitis optica spectrum disorders (NMOSDs) remains unclear. In this study, the CD4(+)CXCR5(+)PD-1(+) Tfh cell population in peripheral blood mononuclear cells (PBMCs) obtained from NMOSD patients, age- and gender-matched healthy controls, and multiple sclerosis patients was compared by flow cytometry. The serum levels of IL-21, IL-6, IL-17, TNF-α and IL-10 were analyzed by ELISA assays. We found that in NMOSD, the Tfh cell frequency is higher than that of healthy subjects and multiple sclerosis (MS) patients. There are more Tfh cells in the relapsing stage than the remitting stage of NMOSD, thus demonstrating the close association of the Tfh cell population with disease activity. Methylprednisolone, which is used to control disease relapses, significantly decreased the proportion of Tfh cells in NMOSD patients. Copyright © 2014 Elsevier B.V. All rights reserved.
    Journal of Neuroimmunology 11/2014;
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    ABSTRACT: Microglia mediated neuroinflammation plays a crucial role in intracerebral hemorrhage (ICH). Therefore, the negative feedback immune mechanism to keep microglia homeostasis and inhibit the related inflammatory injury is important. Scavenger receptor A (SRA), a pattern recognition molecule, is a physiologic negative regulator of immune consequences. However, its role in microglia mediated immune response has not been well defined. In this study, we detected SRA expression and inflammatory response of microglia treated with erythrocyte lysate in vitro, and observed the cerebral water content and neurological deficit of ICH mice in vivo. We found that SRA was highly expressed in erythrocyte lysate treated microglia. Interestingly, genetic SRA ablation increased microglia activation and cytokine production, and sensitized mice to ICH induced neuron injury. In addition, we adoptive transferred microglia (WT) into ICH mice (SRA-/-), and found that the ICH-induced inflammation injury was effectively ameliorated. Therefore, the results demonstrated that SRA could attenuate microglia mediated inflammation injury in ICH. In addition, SRA mediated negative feedback mechanism in neuroimmune homeostasis might provide a novel therapeutical strategy for ICH. Scavenger receptor SRA restrains T cell activation and protects against concanavalin A-induced hepatic injury. Copyright © 2014. Published by Elsevier B.V.
    Journal of Neuroimmunology 11/2014;