Namgyeong Park

Ms. Namgyeong Park

orcid

Research Focus & Metrics

Academic Career Length

3Years (2024-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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Verified
Journal Article
Open access
PDF file
HYHyeJin Yang
HyeJin Yang
JYJuwon Yang
Juwon Yang
NPNamgyeong Park
Namgyeong Park
DHDeok Sang Hwang
Deok Sang Hwang
SPSeon-young Park
Seon-young Park
HBHyunsu Bae
Hyunsu Bae
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.

2 December 2024 in Preprints.org
Verified
Preprint
Open access
PDF file
HYHyeJin Yang
HyeJin Yang
JYJuwon Yang
Juwon Yang
NPNamgyeong Park
Namgyeong Park
DHDeok Sang Hwang
Deok Sang Hwang
SPSeon-young Park
Seon-young Park
HBHyunsu Bae
Hyunsu Bae
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.