N6-induced IL-10+ B Cells in Mice
N6 treatment led to over 95% of B cells expressing IL-10 and the transfer of these cells resulted in remission of experimental autoimmune encephalomyelitis. In mice, these B cells migrated to the CNS and became IL-10+ plasma cells. The therapeutic effect was lost in mice lacking IL-10 receptors in long-lived myeloid cells.
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Why it matters
This research indicates that enhancing IL-10 expression in B cells could be a potential strategy for treating autoimmunity, specifically in the context of central nervous system conditions.
What this does not prove
The study does not demonstrate safety or efficacy in humans and is limited to animal models; the precise mechanism of N6 in human B cells remains unclear.
Next milestone
No next milestone was established from the available source.
Study facts
- Study design
- Not reported
- Participants / samples
- Not reported
- Randomised
- Not reported
- Controlled
- Not reported
- Primary endpoint met
- Not reported
- Relevant MS type
- Not reported
- Publication date
- 2026-10-06
- Evidence reviewed
- Abstract only
- Regulatory approval
- Not reported
- Research areas
- Not classified
Original sources
- Primary evidenceInduced regulatory B cells stably expressing interleukin-10 reverse central nervous system autoimmunity by targeting myeloid cells. ↗DOI: 10.1016/j.immuni.2026.09.006
Supporting passages (5)
publication datePublication date: 2026-10-06
interventionN6-induced B cells accumulated in the central nervous system (CNS) and differentiated into IL-10+ plasma cells, promoting transcriptional and phenotypic changes in myeloid cells within the CNS.
primary endpointTransfer of IL-10+ B cells induced remission of experimental autoimmune encephalomyelitis.
findingsTransfer of IL-10+ B cells induced remission of experimental autoimmune encephalomyelitis.
limitationsTitle: Induced regulatory B cells stably expressing interleukin-10 reverse central nervous system autoimmunity by targeting myeloid cells.
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