ArticleScientific reports2019
Type I interferon signaling before hematopoietic stem cell transplantation lowers donor T cell activation via reduced allogenicity of recipient cells.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Recent advances in nanoparticles-based sonodynamic and immune checkpoint blockade synergistic therapy for pancreatic ductal adenocarcinoma.Materials today. Bio · 2025Review
- Review
- Bacteria and bacteriophage consortia are associated with protective intestinal metabolites in patients receiving stem cell transplantation.Nature cancer · 2024Article
- CD11c participates in triggering acute graft-versus-host disease during bone marrow transplantation.Immunology · 2021Article
- Review
- Interfering With Inflammation: Heterogeneous Effects of Interferons in Graft-Frontiers in immunology · 2021Review
- STING differentially regulates experimental GVHD mediated by CD8 versus CD4 T cell subsets.Science translational medicine · 2020Article
- Tolerizing Strategies for the Treatment of Autoimmune Diseases: FromFrontiers in immunology · 2020Review
- Broad Virus Detection and Variant Discovery in Fecal Samples of Hematopoietic Transplant Recipients Using Targeted Sequence Capture Metagenomics.Frontiers in microbiology · 2020Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies highlight immunoregulatory functions of type I interferons (IFN-I) during the pathogenesis of graft-versus-host disease (GVHD) after allogeneic hematopoietic stem cell transplantation (allo-HSCT). We demonstrated that selective activation of IFN-I pathways including RIG-I/MAVS and cGAS/STING prior to allo-HSCT conditioning therapy can ameliorate the course of GVHD. However, direct effects of IFN-Is on immune cells remain ill characterized. We applied RIG-I agonists (3pRNA) to stimulate IFN-I production in murine models of conditioning therapy with total body irradiation (TBI) and GVHD. Using IFN-I receptor-deficient donor T cells and hematopoietic cells, we found that endogenous and RIG-I-induced IFN-Is do not reduce GVHD by acting on these cell types. However, 3pRNA applied before conditioning therapy reduced the ability of CD11c
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