ArticleEMBO reports2025
CD47-amyloid-β-CD74 signaling triggers adaptive immunosuppression in sepsis.
Article in EMBO reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
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Who cites it
4 citing papers in PubMed.
- Biomimetic Targeted Drug Delivery for Liver Failure in Abdominal Sepsis: Focus on Autologous Erythrocyte Ghosts.International journal of molecular sciences · 2026Review
- The Dual Role of Natural Killer Cells in the Septic Liver.Journal of inflammation research · 2026Review
- The single-cell immune atlas of bacterial pneumonia: from inflammatory cell infiltration to treatable cell states.Frontiers in cellular and infection microbiology · 2026Review
- Immunomodulatory therapy for sepsis: from pathophysiological mechanisms to precision treatment.Frontiers in cellular and infection microbiology · 2025Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. However, how this dysregulation occurs remains to be elucidated. In this study, we use single-cell RNA sequencing (scRNA-seq) and conventional RNA-seq to analyze the immune landscape of sepsis and observe that adaptive immunity is acutely and strongly suppressed. This systemic immunosuppression occurs not only in the peripheral blood but also in all other immune compartments, including the spleen, lymph nodes, and bone marrow. Clinical data show that these adaptive immunity-related genes may have the potential to be used to distinguish patients with sepsis from those with common infections. CD47 is found to play a pivotal role in this immunosuppression by inducing the production of amyloid-β (Aβ), which interacts with CD74 on B cells, leading to B-cell suppression and subsequent adaptive immunosuppression. Blocking CD47-Aβ signaling significantly reduces organ injury and improves the survival rate of septic mice by restoring phagocytic cell functions and alleviating B-cell suppression and adaptive immunosuppression.
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Registered trials
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