Erschienen:
Proceedings of the National Academy of Sciences, 2016
Erschienen in:
Proceedings of the National Academy of Sciences, 113 (2016) 12, Seite 3323-3328
Sprache:
Englisch
DOI:
10.1073/pnas.1519608113
ISSN:
0027-8424;
1091-6490
Entstehung:
Anmerkungen:
Beschreibung:
SignificanceAlthough T cells are the main players in autoimmune CNS inflammation, the role of B cells is being increasingly appreciated. We here investigated possible scenarios of how B cells could participate in the initiation of autoimmune CNS disease. We show that myelin-reactive autoantibodies accumulate in CNS-resident phagocytes, thereby concentrating myelin antigens in these cells and increasing the cells’ capacity to present the autoantigen to invading myelin-reactive T cells. Consequently, these T cells are stimulated and more easily reach the threshold for clinically relevant reactivation within the CNS tissue. This previously unidentified mechanism is of potential clinical relevance because it provides a scientific explanation for immune processes leading to disease initiation and induction of relapses in multiple sclerosis and other autoimmune CNS disorders.