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Items 1 to 10 of about 316603
1. Fewings N, Gatt PN, McKay FC, Parnell GP, Schibeci SD, Edwards J, Basuki MA, Goldinger A, Fabis-Pedrini MJ, Kermode AG, Manrique CP, McCauley JL, Nickles D, Baranzini SE, Burke T, Vucic S, Stewart GJ, Booth DR: Data characterizing the ZMIZ1 molecular phenotype of multiple sclerosis. Data Brief; 2017 Apr;11:364-370
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Data characterizing the ZMIZ1 molecular phenotype of multiple sclerosis.
  • The data presented in this article are related to the research article entitled "The autoimmune risk gene ZMIZ1 is a vitamin D responsived marker of a molecular phenotype of multiple sclerosis" Fewings et al. (2017) [1].
  • Here we identify the set of genes correlated with ZMIZ1 in multiple cohorts, provide phenotypic details on those cohorts, and identify the genes negatively correlated with ZMIZ1 and the cells predominantly expressing those genes.

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  • (PMID = 28275670.001).
  • [Journal-full-title] Data in brief
  • [ISO-abbreviation] Data Brief
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS088155
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Keywords] NOTNLM ; Gene expression / Molecular phenotype / Multiple sclerosis / ZMIZ1
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2. Allan ERO, Campden RI, Ewanchuk BW, Tailor P, Balce DR, McKenna NT, Greene CJ, Warren AL, Reinheckel T, Yates RM: A role for cathepsin Z in neuroinflammation provides mechanistic support for an epigenetic risk factor in multiple sclerosis. J Neuroinflammation; 2017 May 10;14(1):103
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A role for cathepsin Z in neuroinflammation provides mechanistic support for an epigenetic risk factor in multiple sclerosis.
  • BACKGROUND: Hypomethylation of the cathepsin Z locus has been proposed as an epigenetic risk factor for multiple sclerosis (MS).
  • METHODS: Experimental autoimmune encephalomyelitis (EAE) was induced in both wildtype mice and mice deficient in cathepsin Z.
  • Consistently, we found that cathepsin Z-deficiency reduced the efficiency of antigen presenting cells to secrete IL-1β, which in turn reduced the ability of mice to generate Th17 responses-critical steps in the pathogenesis of EAE and MS.

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  • (PMID = 28486971.001).
  • [ISSN] 1742-2094
  • [Journal-full-title] Journal of neuroinflammation
  • [ISO-abbreviation] J Neuroinflammation
  • [Language] eng
  • [Publication-type] Journal Article
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3. Singh AK, Novakova L, Axelsson M, Malmeström C, Zetterberg H, Lycke J, Cardell SL: High Interferon-γ Uniquely in Vδ1 T Cells Correlates with Markers of Inflammation and Axonal Damage in Early Multiple Sclerosis. Front Immunol; 2017;8:260

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High Interferon-γ Uniquely in Vδ1 T Cells Correlates with Markers of Inflammation and Axonal Damage in Early Multiple Sclerosis.
  • We have identified a population of T lymphocytes in peripheral blood, Vδ1 TCRγδ T lymphocytes, which unexpectedly was uniquely expressing high production of interferon-γ in newly diagnosed, untreated multiple sclerosis (MS) patients.
  • IFN-γ production in this population distinctly correlated to parameters of clinical disease activity, inflammation, and neuronal damage.
  • A biomarker and early sign of demyelinating disease in MS is much warranted and would help identify immunopathogenesis and prognosis of disease as well as monitor success with adequate treatment.
  • The present study identifies the Vδ1 T lymphocytes as an early marker of MS and a possible link to understanding the disease etiology.

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  • (PMID = 28337205.001).
  • [Journal-full-title] Frontiers in immunology
  • [ISO-abbreviation] Front Immunol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Keywords] NOTNLM ; Vdelta1 T cells / cerebrospinal fluid / gamma-delta T cells / interferon-gamma / multiple sclerosis / natalizumab
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4. Preiningerova JL, Vachova M: Daclizumab high-yield process in the treatment of relapsing-remitting multiple sclerosis. Ther Adv Neurol Disord; 2017 Jan;10(1):67-75

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Daclizumab high-yield process in the treatment of relapsing-remitting multiple sclerosis.
  • Daclizumab is a humanized monoclonal antibody that binds to the α subunit (CD25) of the interleukin-2 receptor and favorably modulates the immune environment in multiple sclerosis (MS).
  • Blockage of CD25, among other effects, causes expansion and enhanced function of regulatory CD56<sup>bright</sup> natural killer cells, which seems to be the leading mechanism of action in MS.
  • Phase II and III clinical trials have demonstrated that monthly subcutaneous injections of daclizumab high yield process (DAC HYP) 150 mg in patients with relapsing MS led to a significant reduction of annualized relapse rate and decreased number of contrast-enhanced lesions on brain magnetic resonance imaging.
  • This review summarizes the development of and clinical experience with daclizumab in MS.

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  • (PMID = 28450896.001).
  • [ISSN] 1756-2856
  • [Journal-full-title] Therapeutic advances in neurological disorders
  • [ISO-abbreviation] Ther Adv Neurol Disord
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Keywords] NOTNLM ; CD25 / daclizumab / interleukin 2 / multiple sclerosis
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5. Zandee SEJ, O'Connor RA, Mair I, Leech MD, Williams A, Anderton SM: IL-10-producing, ST2-expressing Foxp3&lt;sup&gt;+&lt;/sup&gt; T cells in multiple sclerosis brain lesions. Immunol Cell Biol; 2017 May;95(5):484-490

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IL-10-producing, ST2-expressing Foxp3<sup>+</sup> T cells in multiple sclerosis brain lesions.
  • CD4<sup>+</sup>Foxp3<sup>+</sup> T regulatory (Treg) cells provide a key defence against inflammatory disease, but also have an ability to produce pro-inflammatory cytokines.
  • The evidence for these two possibilities in multiple sclerosis (MS) is controversial.
  • We show that Foxp3<sup>+</sup> cells in the brains of MS patients predominantly produce interleukin-10 (IL-10) and show high expression of the IL-33 receptor ST2 (associated with potent Treg function), indicating that Treg in the inflamed brain maintain their suppressive function.

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  • (PMID = 28169287.001).
  • [ISSN] 1440-1711
  • [Journal-full-title] Immunology and cell biology
  • [ISO-abbreviation] Immunol. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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6. Marnetto F, Valentino P, Caldano M, Bertolotto A: Detection of potassium channel KIR4.1 antibodies in Multiple Sclerosis patients. J Immunol Methods; 2017 Jun;445:53-58

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of potassium channel KIR4.1 antibodies in Multiple Sclerosis patients.
  • The presence of KIR4.1 antibodies has been proposed to be a characteristic of Multiple Sclerosis (MS).
  • This could have a significant impact on disease management.
  • The aim of this study is to verify the presence of KIR4.1 antibodies in MS patients, by independently replicating the originally-described procedure.
  • Sera of 48 MS patients and 46 HCs were studied in 21 working sessions.
  • In a preliminary analysis, we observed different KIR4.1 antibody levels between MS patients and Healthy Controls (HCs).
  • However, a high variability across working sessions was observed and the sensitivity of the assay was very low.
  • As per these criteria, we detected LG-KIR4.1 antibodies in 28% of MS patients and 5% of HCs.
  • We propose further efforts be made towards the development of a uniform method to establish the detection of KIR4.1 antibodies in MS patients.

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  • [Copyright] Copyright © 2017 Elsevier B.V. All rights reserved.
  • (PMID = 28300540.001).
  • [ISSN] 1872-7905
  • [Journal-full-title] Journal of immunological methods
  • [ISO-abbreviation] J. Immunol. Methods
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Keywords] NOTNLM ; Acceptance criteria / Antigen purification / ELISA / KIR4.1 antibodies / Multiple sclerosis
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7. Mazdeh M, Noroozi R, Gharesouran J, Sayad A, Komaki A, Eftekharian MM, Habibi M, Toghi M, Taheri M: The Importance of VEGF-KDR Signaling Pathway Genes should Not Be Ignored When the Risk of Developing Multiple Sclerosis is Taken into Consideration. J Mol Neurosci; 2017 May;62(1):73-78

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The Importance of VEGF-KDR Signaling Pathway Genes should Not Be Ignored When the Risk of Developing Multiple Sclerosis is Taken into Consideration.
  • Vascular endothelial growth factor (VEGF) and its receptor kinase insert domain-containing receptor (KDR) pathway trigger the process of angiogenesis as well as inflammation, which contributes to the development and progression of demyelinating lesions in multiple sclerosis.
  • This work is a case-control study comprising of a total of 400 subjects with multiple sclerosis and 400 healthy controls.
  • A significantly higher frequency of the T allele and TT genotype of the VEGF 936C > T (rs3025039) polymorphism was found in the multiple sclerosis group than in the healthy control group (P = 0.01 [OR = 1.41] and P = 0.01 [OR = 3.12], respectively).
  • Taken together, the results of the present study suggests that the T allele of the rs3025039 in VEGF gene could be considered a risk factor for developing multiple sclerosis in the Iranian population.

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  • (PMID = 28401369.001).
  • [ISSN] 1559-1166
  • [Journal-full-title] Journal of molecular neuroscience : MN
  • [ISO-abbreviation] J. Mol. Neurosci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; KDR / Multiple sclerosis / Polymorphism / VEGF
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8. Ayuso T, Aznar P, Soriano L, Olaskoaga A, Roldán M, Otano M, Ajuria I, Soriano G, Lacruz F, Mendioroz M: Vitamin D receptor gene is epigenetically altered and transcriptionally up-regulated in multiple sclerosis. PLoS One; 2017;12(3):e0174726

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vitamin D receptor gene is epigenetically altered and transcriptionally up-regulated in multiple sclerosis.
  • OBJECTIVE: Vitamin D deficiency has been linked to increased risk of multiple sclerosis (MS) and poor outcome.
  • However, the specific role that vitamin D plays in MS still remains unknown.
  • In order to identify potential mechanisms underlying vitamin D effects in MS, we profiled epigenetic changes in vitamin D receptor (VDR) gene to identify genomic regulatory elements relevant to MS pathogenesis.
  • METHODS: Human T cells derived from whole blood by negative selection were isolated in a set of 23 relapsing-remitting MS (RRMS) patients and 12 controls matched by age and gender.
  • CONCLUSIONS: An alternative promoter of the VDR gene shows altered DNA methylation levels in patients with multiple sclerosis, and it is associated with VDR mRNA upregulation.
  • This locus may represent a candidate regulatory element in the genome relevant to MS pathogenesis.

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  • (PMID = 28355272.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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9. Farrokhi M, Masoudifar A, Derakhshan A, Saadatmand S, Rouhi-Boroujeni H, Etemadifar M, Rezaei-Zarji S, Javid A, Nobakht R, Deyhimi M, Ekramnia A, Ebrahimi M, Sheikh S, Ansaripour S, Amani-Beni A, Jahanbani-Ardakani H: The Association of Interleukin-16 Gene Polymorphisms with IL-16 Serum Levels and Risk of Multiple Sclerosis. Immunol Invest; 2017 Feb 02;:1-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The Association of Interleukin-16 Gene Polymorphisms with IL-16 Serum Levels and Risk of Multiple Sclerosis.
  • BACKGROUND: Multiple sclerosis (MS) is a chronic inflammatory, demyelinating, and neurodegenerative disease of the central nervous system (CNS) that is immunologically mediated in genetically susceptible individuals.
  • Single-nucleotide polymorphisms (SNPs) in the IL-16 gene may lead to altered cytokine expression or biological activity, and these variations may modulate an individual's risk for MS.
  • To test this hypothesis, we investigated association of IL-16 gene SNPs (i.e., rs4072111 C/T, rs11556218 G/T, and rs4778889 C/T) and serum IL-16 levels with risk of MS in an Iranian population.
  • METHODS: We analyzed the three SNPs of IL-16 in 250 MS patients and 400 healthy controls using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP).
  • The serum level of IL-16 was assessed by enzyme-linked immunosorbent assay (ELISA).
  • RESULTS: The IL-16 rs4072111C/T genotype and allele frequencies showed significantly differences between MS patients and controls (p < 0.01).
  • The mean serum levels of IL-16 in MS patients were significantly higher in MS patients compared to healthy controls (p ≤ 0.01).
  • CONCLUSION: In summary, the present study provides the first evidence that the rs11556218T/G and rs4072111C/T polymorphisms of IL-16 gene were significantly associated with increased risk of MS.
  • These results suggest that rs11556218T/G, rs4072111C/T, and rs4778889T/C polymorphisms of IL-16 may contribute to susceptibility to MS through increased expression of IL-16 levels.

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  • (PMID = 28151028.001).
  • [ISSN] 1532-4311
  • [Journal-full-title] Immunological investigations
  • [ISO-abbreviation] Immunol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Keywords] NOTNLM ; ELISA / interleukin-16 / multiple sclerosis / polymerase chain reaction / polymorphism
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10. Liu G, Hu Y, Jin S, Jiang Q: Genetic variant rs763361 regulates multiple sclerosis CD226 gene expression. Proc Natl Acad Sci U S A; 2017 Feb 07;114(6):E906-E907

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic variant rs763361 regulates multiple sclerosis CD226 gene expression.

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  • (PMID = 28137889.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] United States
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