Evidence map›Paper›PMID 39769442›Full record

ArticleInternational journal of molecular sciences2024

Adoptive Transfer of CX3CR1-Transduced Tregs Homing to the Forebrain in Lipopolysaccharide-Induced Neuroinflammation and 3xTg Alzheimer's Disease Models.

Hyejin Yang, Juwon Yang, Namgyeong Park, Deok-Sang Hwang, Seon-Young Park, Soyoung Kim, Hyunsu Bae

Abstract read
In one paragraph

Article in International journal of molecular sciences, 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. Single-Cell Profiling Reveals Clonally Expanded CX3CR1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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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

7 authors.

Hyejin YangDepartment of Physiology, College of Korean Medicine, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemoon-gu, Seoul 02447, Republic of Korea.ORCID 0000-0003-1742-593X
Juwon YangDepartment of Physiology, College of Korean Medicine, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemoon-gu, Seoul 02447, Republic of Korea.ORCID 0009-0008-8460-8027
Namgyeong ParkDepartment of Clinical Korean Medicine, Graduate School, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemoon-gu, Seoul 02447, Republic of Korea.ORCID 0009-0001-0884-3091
Deok-Sang HwangDepartment of Clinical Korean Medicine, Graduate School, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemoon-gu, Seoul 02447, Republic of Korea.ORCID 0000-0001-9179-0797
Seon-Young ParkDepartment of Physiology, College of Korean Medicine, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemoon-gu, Seoul 02447, Republic of Korea.ORCID 0000-0002-1072-2918
Soyoung KimDepartment of Physiology, College of Korean Medicine, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemoon-gu, Seoul 02447, Republic of Korea.ORCID 0000-0002-2273-0931
Hyunsu BaeDepartment of Physiology, College of Korean Medicine, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemoon-gu, Seoul 02447, Republic of Korea.ORCID 0000-0002-0299-3582

Funding

National Research Foundation of Korea RS-2023-00208347
6 · The paper itself

Abstract

CX3CR1-transduced regulatory T cells (Tregs) have shown potential in reducing neuroinflammation by targeting microglial activation. Reactive microglia are implicated in neurological disorders, and CX3CR1-CX3CL1 signaling modulates microglial activity. The ability of CX3CR1-transduced Tregs to inhibit LPS-induced neuroinflammation was assessed in animal models. CX3CR1 Tregs were administered to LPS-induced and 3xTg Alzheimer's mouse models, resulting in reduced proinflammatory marker expression in both the cortices and hippocampi. In the 3xTg Alzheimer's model, neuroinflammation was significantly reduced, demonstrating the efficacy of CX3CR1 Tregs even in chronic neuroinflammatory conditions. These findings highlight the therapeutic potential of CX3CR1 Treg therapy in modulating microglial activity and offer promising treatment strategies for neurodegenerative diseases.

Indexed as

Alzheimer DiseaseCX3C Chemokine Receptor 1Disease Models, AnimalLipopolysaccharidesNeuroinflammatory DiseasesT-Lymphocytes, RegulatoryAdoptive TransferAnimalsMaleMiceMice, TransgenicMicrogliaProsencephalonCX3C Chemokine Receptor 1Cx3cr1 protein, mouseLipopolysaccharides3xTg mouse modelAlzheimer’s diseaselipopolysaccharidemicroglianeurodegenerationneuroinflammationregulatory T cell

Identifiers

PMID39769442
PMCPMC11727661

What OpenQuestion holds

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Registered trials

None linked

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.