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Kolland, D. ; Kuhlmann, M.* ; de Almeida, G.P.* ; Köhler, A. ; Arifovic, A. ; von Strempel, A.* ; Pourjam, M.* ; Bolsega, S.* ; Wurmser, C.* ; Steiger, K.* ; Basic, M.* ; Neuhaus, K.* ; Schmidt-Weber, C.B. ; Stecher, B.* ; Zehn, D.* ; Ohnmacht, C.

A specific microbial consortium enhances Th1 immunity, improves LCMV viral clearance but aggravates LCMV disease pathology in mice.

Nat. Commun. 16:3902 (2025)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Anti-viral immunity can vary tremendously from individual to individual but mechanistic understanding is still scarce. Here, we show that a defined, low complex bacterial community (OMM12) but not the general absence of microbes in germ-free mice leads to a more potent immune response compared to the microbiome of specific-pathogen-free (SPF) mice after a systemic viral infection with LCMV Clone-13. Consequently, gnotobiotic mice colonized with OMM12 have more severe LCMV-induced disease pathology but also enhance viral clearance in the intestinal tract. Mechanistically, single-cell RNA sequencing analysis of adoptively transferred virus-specific T helper cells and endogenous T helper cells in the intestinal tract reveal a stronger pro-inflammatory Th1 profile and a more vigorous expansion in OMM12 than SPF mice. Altogether, our work highlights the causative function of the intestinal microbiome for shaping adaptive anti-viral immunity with implications for vaccination strategies and anti-cancer treatment regimens.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Cd4(+) T-cells; Lymphocytic Choriomeningitis Virus; Thymus-expressed Chemokine; Transcription Factor; Gut Microbiota; Effector; Persistence; Responses; Memory; Mouse
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Zeitschrift Nature Communications
Quellenangaben Band: 16, Heft: 1, Seiten: , Artikelnummer: 3902 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Förderungen TUM Animal Research Center (ARC)
European Research Council (ERC Starting grant)
German Research Foundation
Deutsche Forschungsgemeinschaft (German Research Foundation)