ArticleShock (Augusta, Ga.)2016
Effect of PD-1: PD-L1 in Invariant Natural Killer T-Cell Emigration and Chemotaxis Following Sepsis.
Article in Shock (Augusta, Ga.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
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
18 citing papers in PubMed.
- T cell exhaustion in sepsis: mechanisms, biomarkers, and immune-reversal strategies.Frontiers in immunology · 2026Review
- Mechanisms of immune suppression in sepsis/shock: one investigator's/lab group's experience (SLB 2024 legacy award presentation).Journal of leukocyte biology · 2025Article
- The Novel Role of the Expression of Toll-like Receptors TLR-5, TLR-6, and TLR-9 and Associated Up-Regulation of Programmed Cell Death 1 Receptor (PD-1) and Its Ligand (PD-L1) in Lung Sepsis.International journal of molecular sciences · 2025Article
- Multi-omics analysis reveals neutrophil heterogeneity and key molecular drivers in sepsis-associated acute kidney injury.Frontiers in immunology · 2025Article
- invariant Natural Killer T Cells Modulate the Peritoneal Macrophage Response to Polymicrobial Sepsis.The Journal of surgical research · 2024Article
- A higher number of exhausted local PD1+, but not TIM3+, NK cells in advanced endometriosis.Heliyon · 2024Article
- invariant Natural Killer T cell therapy as a novel therapeutic approach in hematological malignancies.Frontiers in transplantation · 2024Review
- Review
- 4-Octyl itaconate regulates immune balance by activating Nrf2 and negatively regulating PD-L1 in a mouse model of sepsis.International journal of biological sciences · 2022Article
- Cutaneous burn diminishes beneficial effect of intravenously administered mesenchymal stem cells on acute lung injury induced by smoke inhalation in sheep.Burns : journal of the International Society for Burn Injuries · 2020Article
- Increased attrition of memory T cells during sepsis requires 2B4.JCI insight · 2019Article
- A novel role for programmed cell death receptor ligand 2 in sepsis-induced hepatic dysfunction.American journal of physiology. Gastrointestinal and liver physiology · 2019Article
- Group 2 Innate Lymphoid Cells (ILC2s) Are Key Mediators of the Inflammatory Response in Polymicrobial Sepsis.The American journal of pathology · 2018Article
- A novel role for coinhibitory receptors/checkpoint proteins in the immunopathology of sepsis.Journal of leukocyte biology · 2018Review
- Pre-existing malignancy results in increased prevalence of distinct populations of CD4+ T cells during sepsis.PloS one · 2018Article
- Improved survival after induction of sepsis by cecal slurry in PD-1 knockout murine neonates.Surgery · 2017Article
- Program Cell Death Receptor-1-Mediated Invariant Natural Killer T-Cell Control of Peritoneal Macrophage Modulates Survival in Neonatal Sepsis.Frontiers in immunology · 2017Article
- What's New in Shock, May 2016?Shock (Augusta, Ga.) · 2016Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Invariant natural killer T-cells (iNKT) are a subset of T-cells that play a regulatory role in sepsis. Following cecal ligation and puncture (CLP), iNKT cells emigrate from the liver and into the circulation and peritoneum in a manner dependent upon coinhibitory molecule Programmed Cell Death Receptor 1 (PD-1). We hypothesized that the effect of PD-1 on iNKT-cell emigration was dependent upon the direct PD-1:PD-L1 interaction, and that PD-1 and PD-L1 would play a role in chemotaxis and chemokine receptor expression. Adoptive transfer of Vybrant-labeled wild-type (WT) cells showed the donor iNKT cells migrated from the liver to the peritoneum following CLP, but PD-L1 deficient donor iNKT cells did not. In a chemotaxis assay, WT-iNKT cells chemotaxed to CXCL12, but PD-1 and PD-L1 deficient iNKT cells did not. Using flow cytometry to evaluate chemokine receptor expression, peritoneal iNKT expression of CXCR4 increased following CLP in the WT, PD-1, and PD-L1 deficient animals, and CXCR6 increased in the WT and PD-1 deficient animals. In conclusion here we document that the hepatic emigration of iNKT cells following CLP to the peritoneum appears dependent upon the direct PD-1:PD-L1 interaction; however, although PD-1 and PD-L1 appear to play a role in chemotaxis, this is unlikely a reflection of iNKT-cell chemokine receptor expression changes.
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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.