ArticleFrontiers in immunology2022
Fast Maturation of Splenic Dendritic Cells Upon TBI Is Associated With FLT3/FLT3L Signaling.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Endothelial miR-15a/16-1 Regulation of SYNE1 Mediates Structural and Functional Recovery after Traumatic Brain Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Disruption of the angiopoietin-like system connects lipid homeostasis and hypothalamic dysfunction in ALS.BMC medicine · 2026Article
- Systemic inflammation and its associations in acute moderate-severe Traumatic Brain Injury: a cross-sectional study.Brain, behavior, & immunity - health · 2026Article
- Basophils activate splenic B cells and dendritic cells via IL-13 signaling in acute traumatic brain injury.Journal of neuroinflammation · 2025Article
- Multifaceted role of nitric oxide in vascular dementia.Medical gas research · 2025Review
- Article
- Research progress on digestive disorders following traumatic brain injury.Frontiers in immunology · 2024Review
- Enhancing daily living and cognitive functions in traumatic brain injury patients through Orem's self-care theory.Frontiers in neurology · 2024Article
- Traumatic brain injury alters dendritic cell differentiation and distribution in lymphoid and non-lymphoid organs.Journal of neuroinflammation · 2022Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The consequences of systemic inflammation are a significant burden after traumatic brain injury (TBI), with almost all organs affected. This response consists of inflammation and concurrent immunosuppression after injury. One of the main immune regulatory organs, the spleen, is highly interactive with the brain. Along this brain-spleen axis, both nerve fibers as well as brain-derived circulating mediators have been shown to interact directly with splenic immune cells. One of the most significant comorbidities in TBI is acute ethanol intoxication (EI), with almost 40% of patients showing a positive blood alcohol level (BAL) upon injury. EI by itself has been shown to reduce proinflammatory mediators dose-dependently and enhance anti-inflammatory mediators in the spleen. However, how the splenic immune modulatory effect reacts to EI in TBI remains unclear. Therefore, we investigated early splenic immune responses after TBI with and without EI, using gene expression screening of cytokines and chemokines and fluorescence staining of thin spleen sections to investigate cellular mechanisms in immune cells. We found a strong
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Registered trials
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