Abstract
The blood–brain barrier (BBB) serves as a border limiting access of immunoglobulins from the circulation into the brain. This becomes relevant when studying the pathogenesis of antibody-mediated autoimmune CNS disorders. Here, we characterized the BBB dysfunction in a model of mild experimental adoptive transfer autoimmune encephalomyelitis (AT-EAE). We show that large molecules can readily penetrate the BBB between days 3 and 7 after EAE-induction. This model may be valuable for studying putative pathogenic effects of immunoglobulins in the central nervous system.
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Acknowledgments
The authors thank Lydia Biko, Helga Brünner, Barbara Dekant, Verena Wörtmann and Susanne Hellmig for expert technical assistance. This work was supported by research funds of the University of Würzburg (Interdiziplinäres Zentrum für klinische Forschung, IZKF, TP A 45) and by Deutsche Forschungsgemeinschaft (SFB 581, TP A7).
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Boettger, M.K., Weishaupt, A., Geis, C. et al. Mild experimental autoimmune encephalitis as a tool to induce blood–brain barrier dysfunction. J Neural Transm 117, 165–169 (2010). https://doi.org/10.1007/s00702-009-0342-6
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DOI: https://doi.org/10.1007/s00702-009-0342-6