ArticleFrontiers in immunology2022
αDβ2 as a novel target of experimental polymicrobial sepsis.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Molecular scissors for inflamed lungs: targeting ubiquitin-specific peptidases in acute lung injury.Thorax · 2026Article
- Multifaceted, unique role of CD11c in leukocyte biology.Frontiers in immunology · 2025Review
- Humanized anti-CD11d monoclonal antibodies suitable for basic research and therapeutic applications.Antibody therapeutics · 2025Article
- Leukocyte kinetics and bacterial clearance duringAmerican journal of physiology. Lung cellular and molecular physiology · 2025Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Since sepsis was defined three decades ago, it has been a target of intensive study. However, there is no specific sepsis treatment available, with its high mortality and morbidity. αDβ2 (CD11d/CD18) is one of the four β2 integrin members. Its role in sepsis has been limitedly studied. Using an experimental polymicrobial sepsis model, we found that the deficiency of αDβ2 was associated with less lung injury and better outcome, which was in sharp contrast to other β2 integrin member αLβ2 (CD11a/CD18), and αMβ2 (CD11b/CD18). This phenotype was supported by a reduction of bacterial loads in αDβ2 knockout mice. Further analysis showed that the deficiency of αDβ2 led to a reduction of neutrophil cell death as well as an increase in neutrophil phagocytosis in both murine and human systems. Our data showed a unique role of αDβ2 among the β2 integrin members, which would serve as a potential target to improve the outcome of sepsis.
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Registered trials
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