Journal of Neuroimmunology (J NEUROIMMUNOL)

Publisher: International Society for Neuroimmunology, Elsevier

Journal description

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.

Current impact factor: 2.47

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 2.467
2013 Impact Factor 2.786
2012 Impact Factor 3.033
2011 Impact Factor 2.959
2010 Impact Factor 2.901
2009 Impact Factor 2.841
2008 Impact Factor 3.159
2007 Impact Factor 2.92
2006 Impact Factor 2.88
2005 Impact Factor 2.824
2004 Impact Factor 2.704
2003 Impact Factor 3.054
2002 Impact Factor 3.577
2001 Impact Factor 3.342
2000 Impact Factor 3.355
1999 Impact Factor 3.233
1998 Impact Factor 3.285
1997 Impact Factor 2.845
1996 Impact Factor 3.083
1995 Impact Factor 3.639
1994 Impact Factor 3.188
1993 Impact Factor 2.955
1992 Impact Factor 2.964

Impact factor over time

Impact factor

Additional details

5-year impact 2.76
Cited half-life 8.90
Immediacy index 0.48
Eigenfactor 0.01
Article influence 0.76
Website Journal of Neuroimmunology website
Other titles Journal of neuroimmunology
ISSN 0165-5728
OCLC 7629351
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Authors pre-print on any website, including arXiv and RePEC
    • Author's post-print on author's personal website immediately
    • Author's post-print on open access repository after an embargo period of between 12 months and 48 months
    • Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months
    • Author's post-print may be used to update arXiv and RepEC
    • Publisher's version/PDF cannot be used
    • Must link to publisher version with DOI
    • Author's post-print must be released with a Creative Commons Attribution Non-Commercial No Derivatives License
    • Publisher last reviewed on 03/06/2015
  • Classification

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Acquired demyelinating syndromes (ADS) in children evolve either as a monophasic disease diagnosed as acute demyelinating encephalomyelitis (ADEM), transverse myelitis (TM) or optic neuritis (ON), or a multiphasic one with several relapses most often leading to the diagnosis of multiple sclerosis (MS) or neuromyelitis optica (NMO). These neuroinflammatory disorders are increasingly associated with autoantibodies against proteins such as aquaporin-4 in rare instances, and more frequently against myelin oligodendrocyte glycoprotein (MOG). Recently, in adult NMO patients, C5a levels were shown to be elevated in cerebrospinal fluid (CSF) during acute exacerbation. We investigated the CSF levels of anaphylatoxins and pro-inflammatory cytokines, and plasma MOG antibodies in onset samples from children with ADS. Thirty four children presenting with a first episode of ADS, 17 with monophasic ADS (9 with ADEM, 4 with TM and 4 with ON) and 17 with MS, who had paired blood and CSF samples at onset were included and compared to 12 patients with other non-inflammatory neurological disorders (OND). Cytokines and anaphylatoxins in CSF were measured by Cytometric Bead Array immunoassay. MOG antibody titers in plasma were tested by flow cytometry using a stable cell line expressing full-length human MOG. We found a significant increase in C5a levels in the CSF of patients with monophasic ADS (n = 17) compared to OND (n = 12, p = 0.0036) and to MS (n = 17, p = 0.0371). The C5a levels in MS were higher than in OND without reaching significance (p = 0.2). CSF IL-6 levels were significantly increased in monophasic ADS compared to OND (p = 0.0027) and to MS (p = 0.0046). MOG antibody plasma levels were significantly higher in monophasic ADS (p < 0.0001) and, to a lesser extent, in MS compared to OND (p = 0.0023). Plasma MOG antibodies and CSF IL-6 levels were significantly correlated (r = 0.51, p = 0.018). CSF C5a and IL-6 levels are increased in monophasic ADS but not in MS when compared to OND, suggesting that these markers may help to predict monophasic or relapsing fate of ADS at onset. MOG antibody titers, which were higher in monophasic ADS than in MS, correlated with IL-6 levels, but not with C5a, suggesting an association between MOG antibodies and neuroinflammation in pediatric ADS.
    Journal of Neuroimmunology 12/2015; 289:1-7. DOI:10.1016/j.jneuroim.2015.10.002
  • [Show abstract] [Hide abstract]
    ABSTRACT: Although pain and cognitive deficits are widespread and debilitating symptoms of multiple sclerosis (MS), they remain poorly understood. Theiler's murine encephalomyelitis virus (TMEV) infection is an animal model of MS where disease course is exacerbated by prior stressors. Here chronic infection coupled with prior social stress increased pain behavior and impaired hippocampal-dependent memory consolidation during the demyelinating phase of disease in SJL mice. These results suggest that the TMEV model may be useful in investigating pain and cognitive impairments in MS. However, in contrast with prior Balb/cJ studies, stress failed to consistently alter behavioral and physiological indicators of disease course.
    Journal of Neuroimmunology 12/2015; In Press. DOI:10.1016/j.jneuroim.2015.09.005
  • [Show abstract] [Hide abstract]
    ABSTRACT: Migraine is believed to be a chronic neurological disorder with the exact aetiology being unknown. But, there is a debate on the role of immune dysfunction in migraine pathophysiology. Hence, authors made a debut attempt to explore the link between lymphocyte subset populations and migraine. A significant increase in CD4+ and decrease in CD8+ population were observed in migraine patients compared to healthy volunteers. Interestingly, the immunoregulator CD4+CD25+ levels were less in migraine patients compared to the healthy volunteers. The results of the present study indicate that failure of immunoregulation could be implicated in the pathophysiology of migraine.
    Journal of Neuroimmunology 11/2015; 290. DOI:10.1016/j.jneuroim.2015.11.015
  • [Show abstract] [Hide abstract]
    ABSTRACT: Abstract Profile and immunoreactivity of proteins from HPN tissue, and from C. jejuni (O:19) were investigated. Proteins were extracted, separated by SDS-PAGE, their cross reactivity monitored by Western blotting, and identified by nHPLC-nESI-HRMS analysis. Proteins from C. jejuni, at Mw ~ 70 KDa were chaperone/co-chaperone proteins (GroEL, DnaK and HtpG). In the corresponding HPN band were serum albumin, neurofilament light peptide, cytoskeletal keratins and one HSP 70 and one HSP60. These chaperones reciprocally share high primary sequence homology and conservation of their known epitopes. These findings suggest that HSP chaperones may be suitable candidates involved in the molecular mimicry triggering GBS.
    Journal of Neuroimmunology 11/2015; 288. DOI:10.1016/j.jneuroim.2015.11.005

  • Journal of Neuroimmunology 09/2015; 286. DOI:10.1016/j.jneuroim.2015.07.008
  • [Show abstract] [Hide abstract]
    ABSTRACT: Autophagy, a lysosomal degradative pathway that maintains cellular homeostasis, has emerged as an innate immune defense against pathogens. The role of autophagy in the deregulated HIV-infected central nervous system (CNS) is unclear. We have found that HIV-1-induced neuro-glial (neurons and astrocytes) damage involves modulation of the autophagy pathway. Neuro-glial stress induced by HIV-1 led to biochemical and morphological dysfunctions. X4 HIV-1 produced neuro-glial toxicity coupled with suppression of autophagy, while R5 HIV-1-induced toxicity was restricted to neurons. Rapamycin, a specific mTOR inhibitor (autophagy inducer) relieved the blockage of the autophagy pathway caused by HIV-1 and resulted in neuro-glial protection. Further understanding of the regulation of autophagy by cytokines and chemokines or other signaling events may lead to recognition of therapeutic targets for neurodegenerative diseases. Copyright © 2015 Elsevier B.V. All rights reserved.
    Journal of Neuroimmunology 08/2015; 285. DOI:10.1016/j.jneuroim.2015.06.001
  • [Show abstract] [Hide abstract]
    ABSTRACT: Neurosarcoidosis (NS) is a rare condition that may mimic central nervous system (CNS) infection, neoplasia and other inflammatory disorders of the CNS such as multiple sclerosis, encephalitis and vasculitis. Diagnosis is challenging in cases with minimal or absent systemic involvement. Cerebrospinal fluid (CSF) angiotensin-converting enzyme (c-ACE) has been claimed as a valuable diagnostic tool for NS. However, there is little data evaluating its performance in routine clinical practice. We performed a monocentric, retrospective, chart-based study including all patients investigated with a lumbar puncture and c-ACE dosage for suspected NS between 01/01/2006 and 31/12/2012 at the Geneva University Hospital. Receiver-operating characteristic (ROC) curve and area under the curve (AUC) were performed to calculate the optimal cut-off value of c-ACE and to determine the discriminative ability of c-ACE. Of the 440 patients included in the study, 9 were diagnosed with NS on the basis of tissue biopsy. Mean c-ACE was not significantly different between NS and non-NS patients. With a cut-off value of 2 (0-2 vs ≥3), sensitivity and specificity of c-ACE were 66.7% and 67.3%, respectively. In our clinical setting, the sensitivity and specificity of c-ACE for NS diagnosis were relatively poor and of little clinical utility. Copyright © 2015 Elsevier B.V. All rights reserved.
    Journal of Neuroimmunology 08/2015; 285. DOI:10.1016/j.jneuroim.2015.05.020
  • [Show abstract] [Hide abstract]
    ABSTRACT: Vitamin D has immunomodulatory effects in multiple sclerosis (MS). Vitamin D acts through various mechanisms such as secretion of cytokines. Interleukin-17 (IL-17) is a critical interleukin in inflammatory response in MS. This study assessed the effect of oral high dose vitamin D intake on IL-17 levels in MS patients in a double blind randomized clinical trial. 94 patients with a diagnosis of relapsing remitting multiple sclerosis (RRMS) were randomized to two groups. One group received 50,000 IU vitamin D3 every five days for 12weeks. The other group was given placebo. Both groups received interferon-β (IFN-β) treatment. Serum levels of IL-17 were measured at the beginning of the study and after 12weeks. IL-17 serum levels were 56.75±28.72pg/ml and 30.31±75.85pg/ml in the intervention and placebo group at the beginning of the study, respectively (Median±IQR, p=0.338). After 12weeks, IL-17 levels were 58.93±67.93pg/ml and 46.13±94.70pg/ml in the intervention and placebo group, respectively (Median±IQR, p=0.960). The multiple linear regression analysis indicated that the consumption of vitamin D3 was positively and significantly associated with the logarithm of IL-17 measures (β=1.719; p=0.002 and R2=0.91), adjusted by EDSS scores. IL-17 levels showed significant change in RRMS patients after receiving high dose vitamin D3 for 12weeks. Copyright © 2015 Elsevier B.V. All rights reserved.
    Journal of Neuroimmunology 08/2015; 285. DOI:10.1016/j.jneuroim.2015.05.022

  • Journal of Neuroimmunology 08/2015; 287(2015):43-53.
  • [Show abstract] [Hide abstract]
    ABSTRACT: The present study compared lymphocyte and T memory subsets in currently untreated patients with chronic inflammatory demyelinating polyneuropathy (CIDP) to glucocorticosteroid (GS) and intravenous immunoglobulin (IVIG) treated patients. Peripheral blood from 48 CIDP patients (21 untreated who were either treatment naïve or without treatment during the last 3months, 17 IVIG and 10 GS treatment) and from 12 age-matched controls was evaluated using flow cytometric analysis. Our data demonstrate that long-term GS treatment is associated with reduced frequencies of total CD4+ T cells, CD4+ memory subsets and NK cells while long-term IVIG treatment is associated with alterations of the CD8+ memory compartment. Reduction of CD4+ naïve T cell counts may explain the observation that GS treatment induces prolonged clinical remission compared to IVIG treatment. Copyright © 2015 Elsevier B.V. All rights reserved.
    Journal of Neuroimmunology 06/2015; 283. DOI:10.1016/j.jneuroim.2015.03.023
  • [Show abstract] [Hide abstract]
    ABSTRACT: Laquinimod, is a potential oral immunomodulatory drug, for relapsing-remitting multiple sclerosis (RRMS). We analyzed the blood-transcriptional changes in RRMS patients (who participated in the ALLEGRO clinical trial) at one and six months after laquinimod treatment using gene expression microarrays. The molecular effects of laquinimod were enhanced by duration of treatment and showed down-regulation of inflammatory responses mainly via TGFb signaling, and of pro-inflammatory cytokines as well as of cellular movement, including adhesion, migration and leukocyte extravasation signaling. Our results demonstrate that laquinimod suppresses inflammation through down-regulation of inflammatory cytokines and arrest of leukocyte extravasation and thereby could attenuate disease activity in RRMS patients. Copyright © 2015 Elsevier B.V. All rights reserved.
    Journal of Neuroimmunology 06/2015; 283. DOI:10.1016/j.jneuroim.2015.04.007
  • [Show abstract] [Hide abstract]
    ABSTRACT: In this study we examined Th1 and Th17 immune responses to rat myelin basic protein (MBP), bovine MBP, human MBP, MBP 68-86, MBP 63-81 and ovalbumin in Lewis rats to determine which MBP antigen is recognized following ischemic brain injury. Responses were compared to animals immunized to rat MBP. Data show that immune responses following immunization with rat MBP are promiscuous with cross reaction to MBP from other species. After stroke, few animals develop Th1 or Th17 responses to MBP, but when those responses occur, especially Th1 responses to rat MBP in the brain, they are predictive of worse stroke outcome. Copyright © 2015 Elsevier B.V. All rights reserved.
    Journal of Neuroimmunology 05/2015; 285. DOI:10.1016/j.jneuroim.2015.05.024