ArticleFrontiers in immunology2020
Type 1 Interferon Gene Signature Promotes RBC Alloimmunization in a Lupus Mouse Model.
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- The Nrf2 Activator CDDO-Imidazole Suppresses Inflammation-Induced Red Blood Cell Alloimmunization.Antioxidants (Basel, Switzerland) · 2025Article
- The involvement of mitochondria in erythrocyte pathology and diseases: from mechanisms to therapeutic strategies.Clinical and experimental medicine · 2025Review
- CDDO-Imidazole regulates RBC alloimmunization to the KEL antigen by activating Nrf2.bioRxiv : the preprint server for biology · 2025Article
- Article
- Research progress in RBC alloimmunization.Frontiers in immunology · 2025Review
- Harnessing the potential of red blood cells in immunotherapy.Human immunology · 2024Review
- Complement C3 and marginal zone B cells promote IgG-mediated enhancement of RBC alloimmunization in mice.The Journal of clinical investigation · 2024Article
- Reticulocytes in donor blood units enhance red blood cell alloimmunization.Haematologica · 2023Article
- Alloantigen Copy Number as a Critical Factor in RBC Alloimmunization.Transfusion medicine reviews · 2023Review
- Distinct RBC alloantibody responses in type 1 interferon-dependent and -independent lupus mouse models.Frontiers in immunology · 2023Article
- Retention of functional mitochondria in mature red blood cells from patients with sickle cell disease.British journal of haematology · 2022Article
- Innate and Adaptive Immunity to Transfused Allogeneic RBCs in Mice Requires MyD88.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Altered type 1 interferon responses in alloimmunized and nonalloimmunized patients with sickle cell disease.EJHaem · 2021Article
- Potential Implications of a Type 1 Interferon Gene Signature on COVID-19 Severity and Chronic Inflammation in Sickle Cell Disease.Frontiers in medicine · 2021Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Red blood cell (RBC) transfusion exposes recipients to hundreds of unmatched minor RBC antigens. This exposure can lead to production of alloantibodies that promote clinically significant hemolytic events. Multiple studies have reported an increased frequency of RBC alloimmunization in patients with autoimmunity. However, cellular and molecular mechanisms that underlie autoimmunity-induced alloimmunization have not been reported. Patients with systemic lupus erythematosus (SLE) have a high frequency of alloimmunization and express a type 1 interferon (IFNα/β) gene signature. Thus, we utilized the pristane-induced lupus mouse model to test the hypothesis that inflammation in lupus promotes RBC alloimmunization, and to examine the potential role of IFNα/β. Intraperitoneal injection of pristane, a hydrocarbon oil, led to autoantibody production, glomerulonephritis, and pulmonary hemorrhage in wild type (WT) mice. Pristane treatment significantly induced serum IFNα and expression of multiple interferon-stimulated genes (ISGs) in peripheral blood and peritoneal fluid cells, including inflammatory macrophages. Following transfusion with allogeneic RBCs expressing the KEL glycoprotein, pristane-treated WT mice produced significantly elevated levels of anti-KEL IgM and anti-KEL IgG, compared to untreated mice. Pristane induced comparable levels of inflammatory cells and cytokines in mice lacking the IFNα/β receptor (IFNAR1
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