Different binding and pathogenic effect of neurofascin and contactin–1 autoantibodies in autoimmune nodopathies
Zitieren Sie bitte immer diese URN: urn:nbn:de:bvb:20-opus-320395
- Introduction IgG4 autoantibodies against paranodal proteins are known to induce acute-onset and often severe sensorimotor autoimmune neuropathies. How autoantibodies reach their antigens at the paranode in spite of the myelin barrier is still unclear. Methods We performed in vitro incubation experiments with patient sera on unfixed and unpermeabilized nerve fibers and in vivo intraneural and intrathecal passive transfer of patient IgG to rats, to explore the access of IgG autoantibodies directed against neurofascin-155 and contactin-1 toIntroduction IgG4 autoantibodies against paranodal proteins are known to induce acute-onset and often severe sensorimotor autoimmune neuropathies. How autoantibodies reach their antigens at the paranode in spite of the myelin barrier is still unclear. Methods We performed in vitro incubation experiments with patient sera on unfixed and unpermeabilized nerve fibers and in vivo intraneural and intrathecal passive transfer of patient IgG to rats, to explore the access of IgG autoantibodies directed against neurofascin-155 and contactin-1 to the paranodes and their pathogenic effect. Results We found that in vitro incubation resulted in weak paranodal binding of anti-contactin-1 autoantibodies whereas anti-neurofascin-155 autoantibodies bound to the nodes more than to the paranodes. After short-term intraneural injection, no nodal or paranodal binding was detectable when using anti-neurofascin-155 antibodies. After repeated intrathecal injections, nodal more than paranodal binding could be detected in animals treated with anti-neurofascin-155, accompanied by sensorimotor neuropathy. In contrast, no paranodal binding was visible in rats intrathecally injected with anti-contactin-1 antibodies, and animals remained unaffected. Conclusion These data support the notion of different pathogenic mechanisms of anti-neurofascin-155 and anti-contactin-1 autoantibodies and different accessibility of paranodal and nodal structures.…
Autor(en): | Katharina Hecker, Julia Grüner, Beate Hartmannsberger, Luise Appeltshauser, Carmen Villmann, Claudia Sommer, Kathrin Doppler |
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URN: | urn:nbn:de:bvb:20-opus-320395 |
Dokumentart: | Artikel / Aufsatz in einer Zeitschrift |
Institute der Universität: | Medizinische Fakultät / Institut für Klinische Neurobiologie |
Medizinische Fakultät / Neurologische Klinik und Poliklinik | |
Medizinische Fakultät / Klinik und Poliklinik für Anästhesiologie (ab 2004) | |
Sprache der Veröffentlichung: | Englisch |
Titel des übergeordneten Werkes / der Zeitschrift (Englisch): | Frontiers in Immunology |
Erscheinungsjahr: | 2023 |
Band / Jahrgang: | 14 |
Aufsatznummer: | 1189734 |
Originalveröffentlichung / Quelle: | Frontiers in Immunology (2023) 14:1189734. https://doi.org/10.3389/fimmu.2023.1189734 |
DOI: | https://doi.org/10.3389/fimmu.2023.1189734 |
Allgemeine fachliche Zuordnung (DDC-Klassifikation): | 6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit / 610 Medizin und Gesundheit |
Freie Schlagwort(e): | IgG4; autoimmune nodopathy; contactin; inflammatory neuropathy; neurofascin; node of ranvier; passive transfer |
Datum der Freischaltung: | 31.05.2024 |
Lizenz (Deutsch): | CC BY: Creative-Commons-Lizenz: Namensnennung 4.0 International |