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  • 1
    Online Resource
    Online Resource
    Assays for Infliximab Drug Levels and Antibodies: A Matter of Scales and Categories
    Wiley ; 2017
    In:  Scandinavian Journal of Immunology Vol. 86, No. 3 ( 2017-09), p. 165-170
    Details
    In: Scandinavian Journal of Immunology, Wiley, Vol. 86, No. 3 ( 2017-09), p. 165-170
    Abstract: Immunogenicity is a frequent cause of secondary non‐response to tumour necrosis factor ( TNF ) inhibitors. Drug level measurement and detection of antidrug antibodies have been shown to be cost effective and clinically relevant, and a large number of assays are available for these purposes. It is, however, difficult to compare assays and translate results into clinical meaningful information due to different methodological approaches and a lack of assay standardization. We have analysed infliximab drug levels and antidrug antibodies in 107 patient samples using enzyme‐linked immunoassays ( ELISA ), immunofluorometric assays ( IFMA ) and reporter‐gene assays ( RGA ). The RGA gave the lowest results for drug levels, whereas the IFMA detected the highest number of antidrug antibody positive sera. Applying individualized therapeutic ranges to each assay resulted in agreement among all three assays in 74% of samples for drug levels and 98% of samples for antidrug antibodies. We found that TNF inhibitor monitoring assays measure on different scales and that the agreement between quantitative results is limited. However, interassay differences can partially be overcome by assay‐individualized translations of quantities into categories, which also is necessary for a meaningful clinical application. Our data demonstrate that assays should not be used interchangeably and that direct comparison of quantitative drug levels obtained with different assays should be avoided.
    Type of Medium: Online Resource
    ISSN: 0300-9475 , 1365-3083
    URL: Issue
    URL: Article
    DOI: 10.1111/sji.2017.86.issue-3
    DOI: 10.1111/sji.12572
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2017
    detail.hit.zdb_id: 2020954-X
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  • 2
    Online Resource
    Online Resource
    Morvan syndrome with Caspr2 antibodies. Clinical and autopsy report
    Elsevier BV ; 2017
    In:  Journal of the Neurological Sciences Vol. 372 ( 2017-01), p. 453-455
    Details
    In: Journal of the Neurological Sciences, Elsevier BV, Vol. 372 ( 2017-01), p. 453-455
    Type of Medium: Online Resource
    ISSN: 0022-510X
    URL: Article
    DOI: 10.1016/j.jns.2016.10.046
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2017
    detail.hit.zdb_id: 1500645-1
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  • 3
    Online Resource
    Online Resource
    CCDC 104 Antibodies and Mitosis of Cancer Cells
    Wiley ; 2018
    In:  Scandinavian Journal of Immunology Vol. 87, No. 2 ( 2018-02), p. 109-110
    Details
    In: Scandinavian Journal of Immunology, Wiley, Vol. 87, No. 2 ( 2018-02), p. 109-110
    Type of Medium: Online Resource
    ISSN: 0300-9475 , 1365-3083
    URL: Issue
    URL: Article
    DOI: 10.1111/sji.2018.87.issue-2
    DOI: 10.1111/sji.12634
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2018
    detail.hit.zdb_id: 2020954-X
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  • 4
    Online Resource
    Online Resource
    Paraneoplastic cerebellar degeneration: Yo antibody alters mitochondrial calcium buffering capacity
    Wiley ; 2019
    In:  Neuropathology and Applied Neurobiology Vol. 45, No. 2 ( 2019-02), p. 141-156
    Details
    In: Neuropathology and Applied Neurobiology, Wiley, Vol. 45, No. 2 ( 2019-02), p. 141-156
    Abstract: Neurodegeneration is associated with dysfunction of calcium buffering capacity and thereby sustained cellular and mitochondrial calcium overload. Paraneoplastic cerebellar degeneration (PCD), characterized by progressive Purkinje neurone degeneration following paraneoplastic Yo antibody internalization and binding to cerebellar degeneration‐related protein CDR2 and CDR2L, has been linked to intracellular calcium homeostasis imbalance due to calbindin D 28k malfunction. Therefore, we hypothesized that Yo antibody internalization affects not only calbindin calcium binding capacity, but also calcium‐sensitive mitochondrial‐associated signalling, causing mitochondrial calcium overload and thereby Purkinje neurone death. Methods Immunohistochemically, we evaluated cerebellar organotypic slice cultures of rat brains after inducing PCD through the application of Yo antibody‐positive PCD patient sera or purified antibodies against CDR2 and CDR2L how pharmacologically biased mitochondrial signalling affected PCD pathology. Results We found that Yo antibody internalization into Purkinje neurons caused depletion of Purkinje neurone calbindin‐immunoreactivity, cannabinoid 1 receptor over‐activation and alterations in the actions of the mitochondria permeability transition pore (MPTP), voltage‐dependent anion channels, reactive oxygen species (ROS) and Na + /Ca 2+ exchangers (NCX). The pathological mechanisms caused by Yo antibody binding to CDR2 or CDR2L differed between the two targets. Yo‐CDR2 binding did not alter the mitochondrial calcium retention capacity, cyclophilin D‐independent opening of MPTP or activity of NCX. Conclusion These findings suggest that minimizing intracellular calcium overload toxicity either directly with cyclosporin‐A or indirectly with cannabidiol or the ROS scavenger butylated hydroxytoluene promotes mitochondrial calcium homeostasis and may therefore be used as future neuroprotective therapy for PCD patients.
    Type of Medium: Online Resource
    ISSN: 0305-1846 , 1365-2990
    URL: Issue
    URL: Article
    DOI: 10.1111/nan.2019.45.issue-2
    DOI: 10.1111/nan.12492
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 2008293-9
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  • 5
    Online Resource
    Online Resource
    Antibody response to seasonal influenza vaccination in patients with multiple sclerosis receiving immunomodulatory therapy
    Wiley ; 2018
    In:  European Journal of Neurology Vol. 25, No. 3 ( 2018-03), p. 527-534
    Details
    In: European Journal of Neurology, Wiley, Vol. 25, No. 3 ( 2018-03), p. 527-534
    Abstract: We have previously shown that patients with multiple sclerosis receiving immunomodulatory treatment have reduced seroprotection rates after influenza immunization. The aim of this study was to further investigate the influence of immunomodulatory therapies on the antibody response and seroprotection rates in patients immunized with seasonal influenza vaccine in 2012/2013 compared with healthy controls. Methods Ninety patients receiving fingolimod, glatiramer acetate, interferon beta‐1a/1b, natalizumab or no therapy were compared with 62 healthy controls. All subjects received the inactivated split virus vaccine in 2012 and serum samples were collected pre‐vaccination and 3, 6 and 12 months post‐vaccination. The vaccine responses were evaluated by the hemagglutination inhibition assay and adjusted for age and gender. Results No significant differences in rates of protection against H1N1 for interferon beta‐1a/1b and glatiramer acetate were observed as compared with controls at 3, 6 and 12 months. Fingolimod provided reduced protection at all time points post‐vaccination, whereas natalizumab displayed reduced protection at 3 and 6 months. Patients without immunomodulation did not display protection rates that were significantly different from the controls at 3 and 12 months. Conclusion These findings suggest that patients with multiple sclerosis receiving fingolimod or natalizumab should be considered for a second dose of the vaccine in cases of insufficient protection. Our results further indicate that new immunomodulatory treatment regimens should be systematically evaluated for their influence on influenza‐specific vaccine responses.
    Type of Medium: Online Resource
    ISSN: 1351-5101 , 1468-1331
    URL: Issue
    URL: Article
    DOI: 10.1111/ene.2018.25.issue-3
    DOI: 10.1111/ene.13537
    Language: English
    Publisher: Wiley
    Publication Date: 2018
    detail.hit.zdb_id: 2020241-6
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  • 6
    Online Resource
    Online Resource
    Prostate cancer, Hu antibodies and paraneoplastic neurological syndromes
    Springer Science and Business Media LLC ; 2016
    In:  Journal of Neurology Vol. 263, No. 5 ( 2016-5), p. 1001-1007
    Details
    In: Journal of Neurology, Springer Science and Business Media LLC, Vol. 263, No. 5 ( 2016-5), p. 1001-1007
    Type of Medium: Online Resource
    ISSN: 0340-5354 , 1432-1459
    URL: Article
    DOI: 10.1007/s00415-016-8090-7
    RVK:
    XA 10000
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2016
    detail.hit.zdb_id: 1421299-7
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