Impaired suppressive effect of FoxP3 regulatory T cells on B cells in multiple sclerosis

B cells are key contributors to the pathogenesis of many autoimmune diseases (AID), including multiple sclerosis (MS), and appear to evade the peripheral tolerance checkpoints that normally maintain immune homeostasis. The fate of B cells at these checkpoints is believed to be regulated by intracell...

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Hauptverfasser: Greeck, Viktoria B. (Verfasst von) , Würthwein, Cornelia (Verfasst von) , Mimura, Karina (Verfasst von) , Mattes, Katharina (Verfasst von) , Kutza, Michael (Verfasst von) , Schirmer, Lucas (Verfasst von) , Fairless, Richard (Verfasst von) , Williams-Fairless, Sarah K. (Verfasst von) , Jarius, Sven (Verfasst von) , Haas, Jürgen (Verfasst von) , Ruprecht, Klemens (Verfasst von) , Wildemann, Brigitte (Verfasst von)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: 02 May 2026
In: Journal of neuroinflammation
Year: 2026, Jahrgang: 23, Pages: 1-20
ISSN:1742-2094
DOI:10.1186/s12974-026-03776-5
Online-Zugang:Verlag, kostenfrei, Volltext: https://doi.org/10.1186/s12974-026-03776-5
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Verfasserangaben:Viktoria B. Greeck, Cornelia Würthwein, Karina Mimura, Katharina Mattes, Michael Kutza, Lucas Schirmer, Richard Fairless, Sarah K. Williams, Sven Jarius, Jürgen Haas, Klemens Ruprecht and Brigitte Wildemann
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Zusammenfassung:B cells are key contributors to the pathogenesis of many autoimmune diseases (AID), including multiple sclerosis (MS), and appear to evade the peripheral tolerance checkpoints that normally maintain immune homeostasis. The fate of B cells at these checkpoints is believed to be regulated by intracellular Ca2+ signaling cascades triggered through engagement of B cell receptors (BCR), and by the suppressive effects of regulatory T cells (Tregs). However, most of the current knowledge about Treg-B cell interaction comes from animal studies, while data from human studies, particularly in the context of AID, are sparse. In contrast, impaired Treg-mediated inhibition of conventional T cells (Tcons) has already been described for several AID, including MS.
Beschreibung:Online veröffentlicht: 2. Mai 2026, Artikelversion: 16. Mai 2026
Gesehen am 09.07.2026
Beschreibung:Online Resource
ISSN:1742-2094
DOI:10.1186/s12974-026-03776-5