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Endoplasmic Reticulum Stress Response Mediator IRE-1α Promotes Host Dendritic Cells in Graft-versus-Host Disease

Hee-Jin Choi1,2,3, Yongxia Wu1,2,3, Brianyell McDaniel Mims4

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Targeting endoplasmic reticulum stress mediator IRE-1α in dendritic cells (DCs) can suppress graft-versus-host disease (GVHD) after transplantation. This approach preserves the graft-versus-leukemia response, offering a promising strategy for improving transplant outcomes.

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Area of Science:

  • Immunology
  • Cell Biology
  • Oncology

Background:

  • Allogeneic hematopoietic cell transplantation is a vital treatment for hematologic malignancies.
  • Graft-versus-host disease (GVHD) and conditioning regimens can induce endoplasmic reticulum (ER) stress.
  • IRE-1α signaling pathway, including spliced XBP-1 (XBP-1s) and RIDD, plays a role in immune responses.

Purpose of the Study:

  • To investigate the role of IRE-1α-XBP-1s signaling in dendritic cell (DC) function and GVHD.
  • To evaluate the therapeutic potential of inhibiting IRE-1α in host DCs for GVHD treatment.
  • To determine the contribution of XBP-1s and RIDD in DC alloreactivity and GVHD pathogenesis.

Main Methods:

  • Utilized DC-specific XBP-1-deficient mice (donors or recipients).
  • Administered an IRE-1α inhibitor (B-I09) to recipient mice prior to transplantation.
  • Assessed DC survival, alloreactivity, T cell proliferation, and GVHD development in vivo and in vitro.

Main Results:

  • XBP-1s in host DCs is critical for GVHD induction but not for graft-versus-leukemia response.
  • IRE-1α inhibition in recipients significantly suppressed GVHD while maintaining anti-leukemia effects.
  • Inhibition of IRE-1α reduced DC survival and alloreactivity, impairing T cell activation and proliferation.
  • Both XBP-1s and RIDD were found to be essential for optimal DC activation and GVHD.

Conclusions:

  • Host DC XBP-1s and RIDD pathways mediated by IRE-1α signaling are crucial for GVHD pathogenesis.
  • Targeting IRE-1α in host DCs represents a potential therapeutic strategy to mitigate GVHD post-transplantation.
  • This approach offers a way to separate the graft-versus-leukemia effect from GVHD, improving transplant efficacy.