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A granulocyte-macrophage colony-stimulating factor and interleukin-15 fusokine induces a regulatory B cell population with immune suppressive properties. | LitMetric

AI Article Synopsis

  • A modified immune factor called GIFT15 suppresses immune responses by affecting signaling in lymphomyeloid cells, specifically through the IL-15 receptor.
  • Treatment of mouse splenocytes with GIFT15 leads to the development of a new type of regulatory B cells (GIFT15 B(reg) cells) that have certain characteristics and produce the anti-inflammatory cytokine IL-10.
  • Infusing these GIFT15 B(reg) cells into mice with autoimmune encephalomyelitis results in complete remission, demonstrating their potential as a novel therapy for autoimmune diseases, although this effect depends on the presence of functional B cells and specific immune components like MHCII and IL-10.

Article Abstract

We have previously shown that a granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-15 (IL-15) 'fusokine' (GIFT15) exerts immune suppression via aberrant signaling through the IL-15 receptor on lymphomyeloid cells. We show here that ex vivo GIFT15 treatment of mouse splenocytes generates suppressive regulatory cells of B cell ontogeny (hereafter called GIFT15 B(reg) cells). Arising from CD19+ B cells, GIFT15 B(reg) cells express major histocompatibility complex class I (MHCI) and MHCII, surface IgM and IgD, and secrete IL-10, akin to previously described B10 and T2-MZP B(reg) cells, but lose expression of the transcription factor PAX5, coupled to upregulation of CD138 and reciprocal suppression of CD19. Mice with experimental autoimmune encephalomyelitis went into complete remission after intravenous infusion of GIFT15 B(reg) cells paralleled by suppressed neuroinflammation. The clinical effect was abolished when GIFT15 B(reg) cells were derived from mmicroMT (lacking B cells), MHCII-knockout, signal transducer and activator of transcription-6 (STAT-6)-knockout, IL-10-knockout or allogeneic splenocytes, consistent with a pivotal role for MHCII and IL-10 by sygeneic B cells for the observed therapeutic effect. We propose that autologous GIFT15 B(reg) cells may serve as a new treatment for autoimmune ailments.

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Source
http://dx.doi.org/10.1038/nm.2003DOI Listing

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