ArticleNature communications2022
PD-L1 negatively regulates antifungal immunity by inhibiting neutrophil release from bone marrow.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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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
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Pooled it
- The immune-microbe-metal triad: a vicious cycle driving biomaterial corrosion in the oral inflammatory microenvironment.Bioactive materials · 2027Review
- CD8+ regulatory T cells shorten neutrophil lifespan to reduce hemorrhagic transformation after ischemic stroke.The Journal of clinical investigation · 2026Article
- The "Double-Edged Sword" of Neutrophils in Trauma: From Pathophysiological Mechanisms to Precision Immunomodulation Strategies.International journal of molecular sciences · 2026Review
- Dual-Targeting, Hybrid Antifungal Agents Targeting Candida albicans-An Overview.Chemical biology & drug design · 2026Review
- Evaluation of neutrophil oxidative burst capacity in relation to major adverse cardiac events and infection in patients with cardiovascular disease.Clinical research in cardiology : official journal of the German Cardiac Society · 2026Article
- Artificial exosomes synergistically reshape sepsis immune homeostasis by modulating neutrophil fate and blocking PD-1/PD-L1.Cell reports. Medicine · 2026Article
- Article
- Research progress of blood-brain barrier penetrating and brain diseases therapy by natural biopolymer - based nanomedicine delivery systems.Materials today. Bio · 2026Review
- [Role of Gut Mycobiome in Lung Cancer Immunotherapy: Mechanisms, Challenges and Translational Prospects].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2026Review
- The pathogenicity and future treatment strategies ofFrontiers in cellular and infection microbiology · 2026Review
- The role of gut mycobiome in responses to cancer immunotherapy.Gut microbes · 2025Review
- Review
- Emergence, function, and therapeutic strategies to target the PD-1/PD-L1 immune checkpoint during pathogenic fungal infections.Virulence · 2025Review
- Early immune response toMicrobiology spectrum · 2025Article
- The Human Mycobiome: Composition, Immune Interactions, and Impact on Disease.International journal of molecular sciences · 2025Review
- EPHA5 regulates antifungal innate immunity by phosphorylating EPHB2 and Dectin-1.PLoS pathogens · 2025Article
- NLRP3 activation induces BBB disruption and neutrophil infiltration via CXCR2 signaling in the mouse brain.Journal of neuroinflammation · 2025Article
- COX-2 inhibition as a therapeutic strategy for bone loss in Staphylococcus aureus osteomyelitis.Molecular medicine (Cambridge, Mass.) · 2025Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Programmed death ligand 1 (PD-L1) has been shown to be inducibly expressed on neutrophils to suppress host immunity during polymicrobial sepsis, virus and parasite infections. However, the role of PD-L1 on neutrophil-mediated antifungal immunity remains wholly unknown. Here, we show that the expression of PD-L1 on murine and human neutrophils was upregulated upon the engagement of C-type lectin receptor Dectin-1 with its ligand β-glucans, exposed on fungal pathogen Candida albicans yeast. Moreover, β-glucan stimulation induced PD-L1 translocation into nucleus to regulate the production of chemokines CXCL1 and CXCL2, which control neutrophil mobilization. Importantly, C. albicans infection-induced expression of PD-L1 leads to neutrophil accumulation in bone marrow, through mediating their autocrine secretion of CXCL1/2. Furthermore, neutrophil-specific deficiency of PD-L1 impaired CXCL1/2 secretion, which promoted neutrophil migration from bone marrow into the peripheral circulation, thereby conferring host resistance to C. albicans infection. Finally, either PD-L1 blockade or pharmacological inhibition of PD-L1 expression significantly increased neutrophil release from bone marrow to enhance host antifungal immunity. Our data together indicate that activation of Dectin-1/PD-L1 cascade by β-glucans inhibits neutrophil release from bone marrow reserve, contributing to the negative regulation of antifungal innate immunity, which functions as a potent immunotherapeutic target against life-threatening fungi infections.
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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.