ArticleShock (Augusta, Ga.)2013
Inflammatory mechanisms in sepsis: elevated invariant natural killer T-cell numbers in mouse and their modulatory effect on macrophage function.
Article in Shock (Augusta, Ga.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 26 citations in OpenAlex.
- Mechanisms of immune suppression in sepsis/shock: one investigator's/lab group's experience (SLB 2024 legacy award presentation).Journal of leukocyte biology · 2025Article
- invariant Natural Killer T Cells Modulate the Peritoneal Macrophage Response to Polymicrobial Sepsis.The Journal of surgical research · 2024Article
- Tertiary peritonitis: considerations for complex team-based care.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2022Review
- The iNKT Cell-Macrophage Axis in Homeostasis and Disease.International journal of molecular sciences · 2022Review
- Harnessing the Versatility of Invariant NKT Cells in a Stepwise Approach to Sepsis Immunotherapy.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Mucosal-associated invariant T (MAIT) cells mediate protective host responses in sepsis.eLife · 2020Article
- Post-sepsis immunosuppression depends on NKT cell regulation of mTOR/IFN-γ in NK cells.The Journal of clinical investigation · 2020Article
- Pathological alteration and therapeutic implications of sepsis-induced immune cell apoptosis.Cell death & disease · 2019Review
- Innate T cells in the intensive care unit.Molecular immunology · 2019Review
- 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
- Lymphocyte integrin expression differences between SIRS and sepsis patients.Irish journal of medical science · 2017Article
- Cl-Amidine Prevents Histone 3 Citrullination and Neutrophil Extracellular Trap Formation, and Improves Survival in a Murine Sepsis Model.Journal of innate immunity · 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
- Effect of PD-1: PD-L1 in Invariant Natural Killer T-Cell Emigration and Chemotaxis Following Sepsis.Shock (Augusta, Ga.) · 2016Article
- Divergent invariant natural killer T-cell response to sepsis of abdominal vs. non-abdominal origin in human beings.Surgical infections · 2015Article
- CD1d- and MR1-Restricted T Cells in Sepsis.Frontiers in immunology · 2015Review
- Targeting the programmed cell death 1: programmed cell death ligand 1 pathway reverses T cell exhaustion in patients with sepsis.Critical care (London, England) · 2014Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Invariant natural killer T cells (iNKT) cells are emerging as key mediators of innate immune cellular and inflammatory responses to sepsis and peritonitis. Invariant natural killer T cells mediate survival following murine septic shock. Macrophages are pivotal to survival following sepsis. Invariant natural killer T cells have been shown to modulate various mediators of the innate immune system, including macrophages. We demonstrate sepsis-inducing iNKT-cell exodus from the liver appearing in the peritoneal cavity, the source of the sepsis. This migration was affected by programmed death receptor 1. Programmed death receptor 1 is an inhibitory immune receptor, reported as ubiquitously expressed at low levels on iNKT cells. Programmed death receptor 1 has been associated with markers of human critical illness. Programmed death receptor 1-deficient iNKT cells failed to demonstrate similar migration. To the extent that iNKT cells affected peritoneal macrophage function, we assessed peritoneal macrophages' ability to phagocytose bacteria. Invariant natural killer T(-/-) mice displayed dysfunctional macrophage phagocytosis and altered peritoneal bacterial load. This dysfunction was reversed when peritoneal macrophages from iNKT(-/-) mice were cocultured with wild-type iNKT cells. Together, our results indicate that sepsis induces liver iNKT-cell exodus into the peritoneal cavity mediated by programmed death receptor 1, and these peritoneal iNKT cells appear critical to regulation of peritoneal macrophage phagocytic function. Invariant natural killer T cells offer therapeutic targets for modulating immune responses and detrimental effects of sepsis.
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