Evidence map›Paper›PMID 38937750›Full record

ArticleJournal of neuroinflammation2024

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.

Jaclyn Iannucci, Reagan Dominy, Shreya Bandopadhyay, E Madison Arthur, Brenda Noarbe, Amandine Jullienne, Margret Krkasharyan, Richard P Tobin, Aleksandr Pereverzev, Samantha Beevers and 7 more

Abstract read
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Article in Journal of neuroinflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed.

  1. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors.

Jaclyn IannucciDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University, Bryan, TX, USA.
Reagan DominyDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University, Bryan, TX, USA.
Shreya BandopadhyayDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University, Bryan, TX, USA.
E Madison ArthurDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University, Bryan, TX, USA.
Brenda NoarbeDivision of Biomedical Sciences, University of California Riverside, Riverside, CA, USA.
Amandine JullienneDivision of Biomedical Sciences, University of California Riverside, Riverside, CA, USA.
Margret KrkasharyanDivision of Biomedical Sciences, University of California Riverside, Riverside, CA, USA.
Richard P TobinDepartment of Surgery, Division of Surgical Oncology, University of Colorado Anschutz Medical Campus, Denver, CO, USA.
Aleksandr PereverzevDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University, Bryan, TX, USA.
Samantha BeeversDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University, Bryan, TX, USA.
Lavanya VenkatasamyDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University, Bryan, TX, USA.
Karienn A SouzaDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University, Bryan, TX, USA.
Daniel C JupiterDepartment of Biostatistics and Data Science, Department of Orthopaedics and Rehabilitation, The University of Texas Medical Branch, Galveston, TX, USA.
Alan DabneyDepartment of Statistics, College of Arts & Sciences, Texas A&M University, College Station, TX, USA.
Andre ObenausDivision of Biomedical Sciences, University of California Riverside, Riverside, CA, USA.
M Karen Newell-RogersDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University, Bryan, TX, USA. mknewellrogers@tamu.edu.
Lee A ShapiroDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University, Bryan, TX, USA. lshapiro@tamu.edu.

Funding

Mechanisms by which CD74 Contributes to Traumatic Brain InjuryR01NS104282 · NINDS · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI NEWELL ROGERS, M. KAREN, SHAPIRO, LEE A. · 2018 to 2022
$2.3M
NIH HHS R01NS104282NINDS NIH HHS R01 NS104282
6 · The paper itself

Abstract

backgroundTraumatic brain injury (TBI) is a significant risk factor for Alzheimer's disease (AD), and accumulating evidence supports a role for adaptive immune B and T cells in both TBI and AD pathogenesis. We previously identified B cell and major histocompatibility complex class II (MHCII)-associated invariant chain peptide (CLIP)-positive B cell expansion after TBI. We also showed that antagonizing CLIP binding to the antigen presenting groove of MHCII after TBI acutely reduced CLIP + splenic B cells and was neuroprotective. The current study investigated the chronic effects of antagonizing CLIP in the 5xFAD Alzheimer's mouse model, with and without TBI.

methods12-week-old male wild type (WT) and 5xFAD mice were administered either CLIP antagonist peptide (CAP) or vehicle, once at 30 min after either sham or a lateral fluid percussion injury (FPI). Analyses included flow cytometric analysis of immune cells in dural meninges and spleen, histopathological analysis of the brain, magnetic resonance diffusion tensor imaging, cerebrovascular analysis, and assessment of motor and neurobehavioral function over the ensuing 6 months.

results9-month-old 5xFAD mice had significantly more CLIP + B cells in the meninges compared to age-matched WT mice. A one-time treatment with CAP significantly reduced this population in 5xFAD mice. Importantly, CAP also improved some of the immune, histopathological, and neurobehavioral impairments in 5xFAD mice over the ensuing six months. Although FPI did not further elevate meningeal CLIP + B cells, it did negate the ability of CAP to reduce meningeal CLIP + B cells in the 5xFAD mice. FPI at 3 months of age exacerbated some aspects of AD pathology in 5xFAD mice, including further reducing hippocampal neurogenesis, increasing plaque deposition in CA3, altering microgliosis, and disrupting the cerebrovascular structure. CAP treatment after injury ameliorated some but not all of these FPI effects.

Indexed as

Antigens, Differentiation, B-LymphocyteB-LymphocytesBrain Injuries, TraumaticHistocompatibility Antigens Class IIMice, TransgenicAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsDisease Models, AnimalHumansMaleMeningesMiceMice, Inbred C57BLPresenilin-1Amyloid beta-Protein PrecursorAntigens, Differentiation, B-LymphocyteHistocompatibility Antigens Class IIinvariant chainPresenilin-1Adaptive immuneAlzheimer’s diseaseCD74CerebrovascularDepressionFluid percussion injuryInnate immuneMHCIINeurobehaviorNeuroinflammation

Identifiers

PMID38937750
PMCPMC11212436

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.