ArticleScientific reports2018
Innate immune system activation in zebrafish and cellular models of Diamond Blackfan Anemia.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Ribosomal protein deficiencies linked to Diamond-Blackfan anemia induce distinctive alterations of ATF4 expression.iScience · 2025Article
- Nucleic acid-induced inflammation on hematopoietic stem cells.Experimental hematology · 2024Article
- Exploring the Effects of Lignin Nanoparticles in Different Zebrafish Inflammatory Models.International journal of nanomedicine · 2024Article
- Review
- Inflammation fuels bone marrow exhaustion caused by Samd9l mutation.The Journal of clinical investigation · 2022Article
- One Host-Multiple Applications: Zebrafish (International journal of molecular sciences · 2022Review
- Decoding the pathogenesis of Diamond-Blackfan anemia using single-cell RNA-seq.Cell discovery · 2022Article
- Proteostasis Perturbations and Their Roles in Causing Sterile Inflammation and Autoinflammatory Diseases.Cells · 2022Review
- Zebrafish models of inflammation in hematopoietic development and disease.Frontiers in cell and developmental biology · 2022Review
- Evaluation of the effects ofToxicology reports · 2022Article
- A new murine Rpl5 (uL18) mutation provides a unique model of variably penetrant Diamond-Blackfan anemia.Blood advances · 2021Article
- Inflammatory Bowel Disease: New Insights into the Interplay between Environmental Factors and PPARγ.International journal of molecular sciences · 2021Review
- Proerythroblast Cells of Diamond-Blackfan Anemia Patients WithFrontiers in physiology · 2021Article
- Minimal role of interleukin 6 and toll-like receptor 2 and 4 in murine models of immune-mediated bone marrow failure.PloS one · 2021Article
- Oxidative DNA Damage, Inflammatory Signature, and Altered Erythrocytes Properties in Diamond-Blackfan Anemia.International journal of molecular sciences · 2020Article
- Diamond Blackfan anemia is mediated by hyperactive Nemo-like kinase.Nature communications · 2020Article
- Article
- Modeling hematopoietic disorders in zebrafish.Disease models & mechanisms · 2019Review
- Zebrafish Models of Rare Hereditary Pediatric Diseases.Diseases (Basel, Switzerland) · 2018Review
- Rare Genetic Blood Disease Modeling in Zebrafish.Frontiers in genetics · 2018Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Deficiency of ribosomal proteins (RPs) leads to Diamond Blackfan Anemia (DBA) associated with anemia, congenital defects, and cancer. While p53 activation is responsible for many features of DBA, the role of immune system is less defined. The Innate immune system can be activated by endogenous nucleic acids from non-processed pre-rRNAs, DNA damage, and apoptosis that occurs in DBA. Recognition by toll like receptors (TLRs) and Mda5-like sensors induces interferons (IFNs) and inflammation. Dying cells can also activate complement system. Therefore we analyzed the status of these pathways in RP-deficient zebrafish and found upregulation of interferon, inflammatory cytokines and mediators, and complement. We also found upregulation of receptors signaling to IFNs including Mda5, Tlr3, and Tlr9. TGFb family member activin was also upregulated in RP-deficient zebrafish and in RPS19-deficient human cells, which include a lymphoid cell line from a DBA patient, and fetal liver cells and K562 cells transduced with RPS19 shRNA. Treatment of RP-deficient zebrafish with a TLR3 inhibitor decreased IFNs activation, acute phase response, and apoptosis and improved their hematopoiesis and morphology. Inhibitors of complement and activin also had beneficial effects. Our studies suggest that innate immune system contributes to the phenotype of RPS19-deficient zebrafish and human cells.
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Registered trials
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