ArticleScientific reports2020
TICAM2-related pathway mediates neutrophil exhaustion.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- Identification of novel sepsis-related neutrophil subsets and surface markers for clinical diagnosis and outcome.Virulence · 2026Article
- Targeting Immune Dysregulation After Burn Injury for Improved Healing and Outcomes.Biomolecules · 2026Review
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- Integrative multiomics analysis reveals the ameliorative effects of Xiasangju on metabolic dysfunction-associated steatohepatitis.Chinese medicine · 2026Article
- Evolocumab Alters Transcriptomic Signatures and Identifies Inflammatory Biomarkers in Brain-Heart Syndrome with Coronary Heart Disease History.International journal of general medicine · 2026Article
- Dual role of CD177 + neutrophils in inflammatory bowel disease: a review.Journal of translational medicine · 2024Review
- Resolving neutrophils through genetic deletion of TRAM attenuate atherosclerosis pathogenesis.iScience · 2024Article
- Sepsis in elderly patients: the role of neutrophils in pathophysiology and therapy.Internal and emergency medicine · 2024Review
- Altered DNA methylation underlies monocyte dysregulation and immune exhaustion memory in sepsis.Cell reports · 2024Article
- Effects of immune exhaustion and senescence of innate immunity in autoimmune disorders.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2024Review
- Resolving neutrophils due to TRAM deletion renders protection against experimental sepsis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Isolation methods determine human neutrophil responses after stimulation.Frontiers in immunology · 2023Article
- TRAM deletion attenuates monocyte exhaustion and alleviates sepsis severity.Frontiers in immunology · 2023Article
- High-resolution single-cell atlas reveals diversity and plasticity of tissue-resident neutrophils in non-small cell lung cancer.Cancer cell · 2022Article
- Generation of resolving memory neutrophils through pharmacological training with 4-PBA or genetic deletion of TRAM.Cell death & disease · 2022Article
- NET Release of Long-Term Surviving Neutrophils.Frontiers in immunology · 2022Article
- Metabolic Pathways Involved in Formation of Spontaneous and Lipopolysaccharide-Induced Neutrophil Extracellular Traps (NETs) Differ in Obesity and Systemic Inflammation.International journal of molecular sciences · 2021Article
- Article
- Development of Exhausted Memory Monocytes and Underlying Mechanisms.Frontiers in immunology · 2021Article
- Single Cell RNA-Seq and Machine Learning Reveal Novel Subpopulations in Low-Grade Inflammatory Monocytes With Unique Regulatory Circuits.Frontiers in immunology · 2021Article
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
Pathogenic inflammation and immune suppression are the cardinal features that underlie the pathogenesis of severe systemic inflammatory syndrome and sepsis. Neutrophil exhaustion may play a key role during the establishment of pathogenic inflammation and immune suppression through elevated expression of inflammatory adhesion molecules such as ICAM1 and CD11b as well as immune-suppressors such as PD-L1. However, the mechanism of neutrophil exhaustion is not well understood. We demonstrated that murine primary neutrophils cultured in vitro with the prolonged lipopolysaccharides (LPS) stimulation can effectively develop an exhaustive phenotype resembling human septic neutrophils with elevated expression of ICAM1, CD11b, PD-L1 as well as enhanced swarming and aggregation. Mechanistically, we observed that TICAM2 is involved in the generation of neutrophil exhaustion, as TICAM2 deficient neutrophils have the decreased expression of ICAM1, CD11b, PD-L1, and the reduced aggregation following the prolonged LPS challenge as compared to wild type (WT) neutrophils. LPS drives neutrophil exhaustion through TICAM2 mediated activation of Src family kinases (SFK) and STAT1, as the application of SFK inhibitor Dasatinib blocks neutrophil exhaustion triggered by the prolonged LPS challenge. Functionally, TICAM2 deficient mice were protected from developing severe systemic inflammation and multi-organ injury following the chemical-induced mucosal damage. Together, our data defined a key role of TICAM2 in facilitating neutrophil exhaustion and that targeting TICAM2 may be a potential approach to treating the severe systemic inflammation.
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