Cheng Li , Xiaopo Gao , Yuan Liu , Bin Yang , Hongkai Dai , Hui Zhao , Yongshen Li
{"title":"The role of natural killer T cells in sepsis-associated acute kidney injury","authors":"Cheng Li , Xiaopo Gao , Yuan Liu , Bin Yang , Hongkai Dai , Hui Zhao , Yongshen Li","doi":"10.1016/j.intimp.2025.114953","DOIUrl":null,"url":null,"abstract":"<div><div>The condition of sepsis, defined by the misregulation of the body's defensive mechanisms against infection, culminates in the potential for catastrophic organ damage and stands as a primary driver of mortality in Intensive Care Units (ICU) settings. Among patients in a critical condition, sepsis is a predominant factor in the development of acute kidney injury (AKI), and the death rate among those with both sepsis and AKI is considerably higher, underscoring the importance of addressing this health crisis. Sepsis-associated acute kidney injury (S-AKI) is a complex process involving inflammation, microcirculatory issues, and metabolic disorders. Among these, the inflammatory response has become a focal point of interest. Bridging the innate and adaptive immunity, natural killer T (NKT) cells can be rapidly activated in sepsis, contributing to sepsis-associated injury and downstream activation of inflammatory cells through the emission of Th1 or Th2 cytokines. They also contribute to S-AKI through the TNF-α/FasL and perforin pathways. Alpha-Galactosylceramide (α-GalCer), acting as a powerful activator for type I NKT (iNKT) cells, is able to regulate the secretory profile of iNKT cells, responding to the pro-inflammatory response and immunosuppressive profiles of sepsis. This review examines the part played by NKT cells in S-AKI and whether α-Galcer could function as a significant regulator in sepsis, based on studies of regression-related mechanisms.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"159 ","pages":"Article 114953"},"PeriodicalIF":4.8000,"publicationDate":"2025-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International immunopharmacology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1567576925009439","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
The condition of sepsis, defined by the misregulation of the body's defensive mechanisms against infection, culminates in the potential for catastrophic organ damage and stands as a primary driver of mortality in Intensive Care Units (ICU) settings. Among patients in a critical condition, sepsis is a predominant factor in the development of acute kidney injury (AKI), and the death rate among those with both sepsis and AKI is considerably higher, underscoring the importance of addressing this health crisis. Sepsis-associated acute kidney injury (S-AKI) is a complex process involving inflammation, microcirculatory issues, and metabolic disorders. Among these, the inflammatory response has become a focal point of interest. Bridging the innate and adaptive immunity, natural killer T (NKT) cells can be rapidly activated in sepsis, contributing to sepsis-associated injury and downstream activation of inflammatory cells through the emission of Th1 or Th2 cytokines. They also contribute to S-AKI through the TNF-α/FasL and perforin pathways. Alpha-Galactosylceramide (α-GalCer), acting as a powerful activator for type I NKT (iNKT) cells, is able to regulate the secretory profile of iNKT cells, responding to the pro-inflammatory response and immunosuppressive profiles of sepsis. This review examines the part played by NKT cells in S-AKI and whether α-Galcer could function as a significant regulator in sepsis, based on studies of regression-related mechanisms.
期刊介绍:
International Immunopharmacology is the primary vehicle for the publication of original research papers pertinent to the overlapping areas of immunology, pharmacology, cytokine biology, immunotherapy, immunopathology and immunotoxicology. Review articles that encompass these subjects are also welcome.
The subject material appropriate for submission includes:
• Clinical studies employing immunotherapy of any type including the use of: bacterial and chemical agents; thymic hormones, interferon, lymphokines, etc., in transplantation and diseases such as cancer, immunodeficiency, chronic infection and allergic, inflammatory or autoimmune disorders.
• Studies on the mechanisms of action of these agents for specific parameters of immune competence as well as the overall clinical state.
• Pre-clinical animal studies and in vitro studies on mechanisms of action with immunopotentiators, immunomodulators, immunoadjuvants and other pharmacological agents active on cells participating in immune or allergic responses.
• Pharmacological compounds, microbial products and toxicological agents that affect the lymphoid system, and their mechanisms of action.
• Agents that activate genes or modify transcription and translation within the immune response.
• Substances activated, generated, or released through immunologic or related pathways that are pharmacologically active.
• Production, function and regulation of cytokines and their receptors.
• Classical pharmacological studies on the effects of chemokines and bioactive factors released during immunological reactions.