ArticleEBioMedicine2016
The Nlrp3 Inflammasome Does Not Regulate Alloimmunization to Transfused Red Blood Cells in Mice.
Article in EBioMedicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Research progress in RBC alloimmunization.Frontiers in immunology · 2025Review
- Erythronecroptosis: an overview of necroptosis or programmed necrosis in red blood cells.Molecular and cellular biochemistry · 2024Review
- The Development and Consequences of Red Blood Cell Alloimmunization.Annual review of pathology · 2023Review
- The inflammasomes: crosstalk between innate immunity and hematology.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Review
- Innate and Adaptive Immunity to Transfused Allogeneic RBCs in Mice Requires MyD88.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Type 1 Interferon Gene Signature Promotes RBC Alloimmunization in a Lupus Mouse Model.Frontiers in immunology · 2020Article
- Structure and function of the immune system in the spleen.Science immunology · 2019Review
- Red blood cell storage lesion: causes and potential clinical consequences.Blood transfusion = Trasfusione del sangue · 2019Review
- B cells require Type 1 interferon to produce alloantibodies to transfused KEL-expressing red blood cells in mice.Transfusion · 2017Article
- Transfusion-related immunomodulation: a reappraisal.Current opinion in hematology · 2017Review
- Type I IFN Is Necessary and Sufficient for Inflammation-Induced Red Blood Cell Alloimmunization in Mice.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Differential Intrasplenic Migration of Dendritic Cell Subsets Tailors Adaptive Immunity.Cell reports · 2016Article
- Red blood cell antigen alloimmunization: Mysteries still unsolved.EBioMedicine · 2016Article
- Transfusion as an Inflammation Hit: Knowns and Unknowns.Frontiers in immunology · 2016Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Red blood cell (RBC) transfusions are essential for patients with hematological disorders and bone marrow failure syndromes. Despite ABO matching, RBC transfusions can lead to production of alloantibodies against "minor" blood group antigens. Non-ABO alloimmunization is a leading cause of transfusion-associated mortality in the U.S. Despite its clinical importance, little is known about the immunological factors that promote alloimmunization. Prior studies indicate that inflammatory conditions place patients at higher risk for alloimmunization. Additionally, co-exposure to pro-inflammatory pathogen associated molecular patterns (PAMPs) promotes alloimmunization in animal models, suggesting that RBC alloimmunization depends on innate immune cell activation. However, the specific innate immune stimuli and sensors that induce a T cell-dependent alloantibody response to transfused RBCs have not been identified. The NLRP3 inflammasome senses chemically diverse PAMPs and damage associated molecular patterns (DAMPs), including extracellular ATP and iron-containing heme. We hypothesized that activation of the NLRP3 inflammasome by endogenous DAMPs from RBCs promotes the alloimmune response to a sterile RBC transfusion. Using genetically modified mice lacking either NLRP3 or multiple downstream inflammasome response elements, we ruled out a role for the NLRP3 inflammasome or any Caspase-1 or -11 dependent inflammasome in regulating RBC alloantibody production to a model antigen.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.