ArticleActa neuropathologica communications2014
Traumatic brain injury causes selective, CD74-dependent peripheral lymphocyte activation that exacerbates neurodegeneration.
Article in Acta neuropathologica communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 69 citations in OpenAlex.
- CD44 antagonism after traumatic brain injury influences the adult neurogenic niche and behavioral outcomes.Brain structure & function · 2026Article
- Neuroimmune Mechanisms in Traumatic Brain Injury and Cancer: Parallel Courses or Existence in Different Orbits.Biomedicines · 2026Review
- Sex differences in neurobehavior and the adult hippocampal neurogenic niche: influence of traumatic brain injury and CLIP antagonism.Frontiers in behavioral neuroscience · 2026Article
- Traumatic brain injury exacerbates alcohol consumption and neuroinflammation with decline in cognition and cholinergic activity.Translational psychiatry · 2025Article
- T Cell Involvement in Neuroinflammation After Traumatic Brain Injury: Implications for Therapeutic Intervention.CNS neuroscience & therapeutics · 2025Review
- Shift work schedules alter immune cell regulation and accelerate cognitive impairment during aging.Journal of neuroinflammation · 2025Article
- Immune Response in Traumatic Brain Injury.Current neurology and neuroscience reports · 2024Review
- Traumatic brain injury alters the effects of class II invariant peptide (CLIP) antagonism on chronic meningeal CLIP + B cells, neuropathology, and neurobehavioral impairment in 5xFAD mice.Journal of neuroinflammation · 2024Article
- Regulatory T lymphocytes in traumatic brain injury.Neurochemistry international · 2024Review
- Context is key: glucocorticoid receptor and corticosteroid therapeutics in outcomes after traumatic brain injury.Frontiers in cellular neuroscience · 2024Review
- Sex-Specific and Traumatic Brain Injury Effects on Dopamine Receptor Expression in the Hippocampus.International journal of molecular sciences · 2023Article
- Dualistic roles and mechanistic insights of macrophage migration inhibitory factor in brain injury and neurodegenerative diseases.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Review
- Therapeutic effects of CD133 + Exosomes on liver function after stroke in type 2 diabetic mice.Frontiers in neuroscience · 2023Article
- Traumatic brain injury with concomitant injury to the spleen: characteristics and mortality of a high-risk trauma cohort from the TraumaRegister DGU®.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2022Article
- Glia as antigen-presenting cells in the central nervous system.Current opinion in neurobiology · 2022Review
- Microglial CD74 Expression Is Regulated by TGFβ Signaling.International journal of molecular sciences · 2022Article
- Unilateral Cervical Vagotomy Modulates Immune Cell Profiles and the Response to a Traumatic Brain Injury.International journal of molecular sciences · 2022Article
- Platelet-to-lymphocyte ratio predicts short-term mortality in patients with moderate to severe traumatic brain injury.Scientific reports · 2022Article
- Brain Trauma, Glucocorticoids and Neuroinflammation: Dangerous Liaisons for the Hippocampus.Biomedicines · 2022Review
- Post-Traumatic Epilepsy and Comorbidities: Advanced Models, Molecular Mechanisms, Biomarkers, and Novel Therapeutic Interventions.Pharmacological reviews · 2022Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionTraumatic brain injury (TBI), a significant cause of death and disability, causes, as in any injury, an acute, innate immune response. A key component in the transition between innate and adaptive immunity is the processing and presentation of antigen by professional antigen presenting cells (APCs). Whether an adaptive immune response to brain injury is beneficial or detrimental is not known. Current efforts to understand the contribution of the immune system after TBI have focused on neuroinflammation and brain-infiltrating immune cells. Here, we characterize and target TBI-induced expansion of peripheral immune cells that may act as potential APCs. Because MHC Class II-associated invariant peptide (CLIP) is important for antigen processing and presentation, we engineered a competitive antagonist (CAP) for CLIP, and tested the hypothesis that peptide competition could reverse or prevent neurodegeneration after TBI.
resultsWe show that after fluid percussion injury (FPI), peripheral splenic lymphocytes, including CD4+ and CD8+ T cells, regulatory T cells (Tregs), and γδ T cells, are increased in number within 24 hours after FPI. These increases were reversed by CAP treatment and this antagonism of CLIP also reduced neuroinflammation and neurodegeneration after TBI. Using a mouse deficient for the precursor of CLIP, CD74, we observed decreased peripheral lymphocyte activation, decreased neurodegeneration, and a significantly smaller lesion size following TBI.
conclusionTaken together, the data support the hypothesis that neurodegeneration following TBI is dependent upon antigen processing and presentation that requires CD74.
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