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Gut microbiota-specific IgA+ B cells traffic to the CNS in active multiple sclerosis

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Sellrie,  Katrin
Biomolekulare Systeme, Max Planck Institute of Colloids and Interfaces, Max Planck Society;

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Seeberger,  Peter H.
Peter H. Seeberger - Vaccine Development, Biomolekulare Systeme, Max Planck Institute of Colloids and Interfaces, Max Planck Society;

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Citation

Pröbstel, A.-K., Zhou, X., Baumann, R., Wischnewski, S., Kutza, M., Rojas, O. L., et al. (2020). Gut microbiota-specific IgA+ B cells traffic to the CNS in active multiple sclerosis. Science Immunology, 5(53): eabc7191. doi:10.1126/sciimmunol.abc7191.


Cite as: http://hdl.handle.net/21.11116/0000-0007-7E2F-9
Abstract
Changes in gut microbiota composition and a diverse role of B cells have recently been implicated in multiple sclerosis (MS), a central nervous system (CNS) autoimmune disease. Immunoglobulin A (IgA) is a key regulator at the mucosal interface. However, whether gut microbiota shape IgA responses and what role IgA+ cells have in neuroinflammation are unknown. Here, we identify IgA-bound taxa in MS and show that IgA-producing cells specific for MS-associated taxa traffic to the inflamed CNS, resulting in a strong, compartmentalized IgA enrichment in active MS and other neuroinflammatory diseases. Unlike previously characterized polyreactive anti-commensal IgA responses, CNS IgA cross-reacts with surface structures on specific bacterial strains but not with brain tissue. These findings establish gut microbiota–specific IgA+ cells as a systemic mediator in MS and suggest a critical role of mucosal B cells during active neuroinflammation with broad implications for IgA as an informative biomarker and IgA-producing cells as an immune subset to harness for therapeutic interventions.