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Läderach, F.* ; Piteros, I.* ; Fennell, E.* ; Bremer, E.* ; Last, M. ; Schmid, S.* ; Rieble, L.* ; Campbell, C.D.* ; Ludwig-Portugall, I.* ; Bornemann, L.* ; Gruhl, A.* ; Eulitz, K.* ; Gueguen, P.* ; Mietz, J.* ; Müller, A.* ; Pezzino, G.* ; Schmitz, J.* ; Ferlazzo, G.* ; Mautner, J. ; Münz, C.*

EBV induces CNS homing of B cells attracting inflammatory T cells.

Nature 646, 171-179 (2025)

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Open Access Green as soon as Postprint is submitted to ZB.

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Epidemiological data have identified Epstein-Barr virus (EBV) infection as the main environmental risk factor for multiple sclerosis, the predominant autoimmune disease of the central nervous system (CNS)¹. However, how EBV infection initiates multiple sclerosis pathogenesis remains unclear. Here we demonstrate that EBV expands oligoclonal T-bet⁺CXCR3⁺ B cells that home to the CNS in humanized mice. Effector memory CD8⁺ T cells and CD4⁺ T_H1 cells as well as CD4⁺ T_H17 cells co-migrate to the brain of EBV-infected humanized mice. T-bet⁺CXCR3⁺ B cells can colonize submeningeal brain regions in the absence of other lymphocytes and attract T cells. Depletion of B cells with rituximab or blocking of CXCR3 significantly decreases lymphocyte infiltration into the CNS. Thus, we suggest that symptomatic primary EBV infection generates B cell subsets that gain access to the CNS, attract T cells and thereby initiate multiple sclerosis.

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Publication type Article: Journal article

Document type Scientific Article

Keywords Epstein-barr-virus; Multiple-sclerosis; Rituximab; Antibody

ISSN (print) / ISBN 0028-0836

e-ISSN 1476-4687

Journal Nature

Quellenangaben Volume: 646, Issue: 8083, Pages: 171-179

Publisher Nature Publishing Group

Publishing Place London

Reviewing status Peer reviewed

Institute(s) Institute of Virology (VIRO)

Grants University of Zurich (Forschungskredit)
Cancer Research Switzerland
Swiss MS Society
Swiss State Secretariat for Education, Research and Innovation for EU
Sobek Foundation
Swiss Vaccine Research Institute
Vontobel Foundation
Roche
Swiss National Science Foundation