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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Gubser, Céline Lindberg, Raija L. P. Sanderson, Nicholas S. R. Eilinger, Luca Schaeren-wiemers, Nicole Zimmermann, Maria Ploegh, Hidde L. Dougan, Stephanie K. Kappos, Ludwig Derfuss, Tobias |
| Description | Author Affiliation: Sanderson NS ( Department of Biomedicine, University Hospital Basel, University of Basel, 4031 Basel, Switzerland); Zimmermann M ( Department of Biomedicine, University Hospital Basel, University of Basel, 4031 Basel, Switzerland.); Eilinger L ( Department of Biomedicine, University Hospital Basel, University of Basel, 4031 Basel, Switzerland.); Gubser C ( Department of Biomedicine, University Hospital Basel, University of Basel, 4031 Basel, Switzerland.); Schaeren-Wiemers N ( Department of Biomedicine, University Hospital Basel, University of Basel, 4031 Basel, Switzerland.); Lindberg RL ( Department of Biomedicine, University Hospital Basel, University of Basel, 4031 Basel, Switzerland.); Dougan SK ( Whitehead Institute for Biomedical Research, Cambridge, MA 02142.); Ploegh HL ( Whitehead Institute for Biomedical Research, Cambridge, MA 02142.); Kappos L ( Department of Biomedicine, University Hospital Basel, University of Basel, 4031 Basel, Switzerland.); Derfuss T ( Clinic of Neurology, Department of Medicine, University Hospital Basel, University of Basel, 4031 Basel, Switzerland.); |
| Abstract | Autoantibodies against myelin oligodendrocyte glycoprotein (MOG) are associated with autoimmune central nervous system diseases like acute disseminated encephalomyelitis (ADEM). For ADEM, it is speculated that a preceding infection is the trigger of the autoimmune response, but the mechanism connecting the infection to the production of MOG antibodies remains a mystery. We reasoned that the ability of B cells to capture cognate antigen from cell membranes, along with small quantities of coexpressed “bystander” antigens, might enable B-cell escape from tolerance. We tested this hypothesis using influenza hemagglutinin as a model viral antigen and transgenic, MOG-specific B cells. Using flow cytometry and live and fixed cell microscopy, we show that MOG-specific B cells take up large amounts of MOG from cell membranes. Uptake of the antigen from the membrane leads to a strong activation of the capturing B cell. When influenza hemagglutinin is also present in the membrane of the target cell, it can be cocaptured with MOG by MOG-specific B cells via the B-cell receptor. Hemagglutinin and MOG are both presented to T cells, which in turn are activated and proliferate. As a consequence, MOG-specific B cells get help from hemagglutinin-specific T cells to produce anti-MOG antibodies. In vivo, the transfer of MOG-specific B cells into recipient mice after the cocapture of MOG and hemagglutinin leads to the production of class-switched anti-MOG antibodies, dependent on the presence of hemagglutinin-specific T cells. This mechanism offers a link between infection and autoimmunity. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 4 |
| Volume Number | 114 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2017-01-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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