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213 results on '"Lim, Dae Seog"'

1. Dendritic Cell-Based Immunotherapy: The Importance of Dendritic Cell Migration.

Author

Song, Min-Seon, Nam, Ji-Hee, Noh, Kyung-Eun, and Lim, Dae-Seog

Subjects
DENDRITIC cells, CELL migration, IMMUNOTHERAPY, IMMUNE response, LYMPH nodes
Abstract

Dendritic cells (DCs) are specialized antigen-presenting cells that are crucial for maintaining self-tolerance, initiating immune responses against pathogens, and patrolling body compartments. Despite promising aspects, DC-based immunotherapy faces challenges that include limited availability, immune escape in tumors, immunosuppression in the tumor microenvironment, and the need for effective combination therapies. A further limitation in DC-based immunotherapy is the low population of migratory DC (around 5%–10%) that migrate to lymph nodes (LNs) through afferent lymphatics depending on the LN draining site. By increasing the population of migratory DCs, DC-based immunotherapy could enhance immunotherapeutic effects on target diseases. This paper reviews the importance of DC migration and current research progress in the context of DC-based immunotherapy. [ABSTRACT FROM AUTHOR]

Published
2024
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8. TNF-α Induces Mitophagy in Rheumatoid Arthritis Synovial Fibroblasts, and Mitophagy Inhibition Alleviates Synovitis in Collagen Antibody-Induced Arthritis

Author

Nam, Ji-Hee, primary, Lee, Jun-Ho, additional, Choi, Hyun-Ji, additional, Choi, So-Yeon, additional, Noh, Kyung-Eun, additional, Jung, Nam-Chul, additional, Song, Jie-Young, additional, Choi, Jinjung, additional, Seo, Han Geuk, additional, Jung, Sang Youn, additional, and Lim, Dae-Seog, additional

Published
2022
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10. BHMPS Inhibits Breast Cancer Migration and Invasion by Disrupting Rab27a-Mediated EGFR and Fibronectin Secretion

Author

Park, Jeong-In, primary, Song, Kyung-Hee, additional, Kang, Seong-Mook, additional, Lee, Jeeyong, additional, Cho, Seong-Jun, additional, Choi, Hyun Kyung, additional, Ahn, Jiyeon, additional, Park, Jong-Kuk, additional, Kim, Jaesung, additional, Hwang, Sang-Gu, additional, Lim, Dae-Seog, additional, Kim, Joon, additional, Jung, Seung-Youn, additional, and Song, Jie-Young, additional

Published
2022
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11. Enpp2 Expression by Dendritic Cells Is a Key Regulator in Migration

Author

Lee, Jun-Ho, primary, Choi, So-Yeon, additional, Park, Soo-Yeoun, additional, Jung, Nam-Chul, additional, Noh, Kyung-Eun, additional, Nam, Ji-Hee, additional, Oh, Ji-Soo, additional, Choi, Hyun-Ji, additional, Jang, Ji-Su, additional, Yoo, Ji-Young, additional, Song, Jie-Young, additional, Seo, Han Geuk, additional, and Lim, Dae-Seog, additional

Published
2021
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23. Asymptomatic Clostridium perfringens Inhabitation in Intestine Can Cause Inflammation, Apoptosis, and Disorders in Brain

Author

Lee, Heeyoung, primary, Lee, Soomin, additional, Kim, Sejeong, additional, Lee, Jeeyeon, additional, Ha, Jimyeong, additional, Choi, Yukyung, additional, Oh, Hyemin, additional, Kim, Yujin, additional, Lee, Yewon, additional, Lim, Dae-Seog, additional, Kim, Saehun, additional, Han, Young Sil, additional, Choi, Kyoung-Hee, additional, and Yoon, Yohan, additional

Published
2020
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26. Pdlim4 is essential for CCR7‐JNK–mediated dendritic cell migration and F‐actin–related dendrite formation

Author

Yoo, Ji-Young, primary, Jung, Nam-Chul, additional, Lee, Jun-Ho, additional, Choi, So-Yeon, additional, Choi, Hyun-Ji, additional, Park, Soo-Yeoun, additional, Jang, Ji-Su, additional, Byun, Sei-Hee, additional, Hwang, Sung-Uk, additional, Noh, Kyung-Eun, additional, Park, Yunok, additional, Lee, Jongwon, additional, Song, Jie-Young, additional, Seo, Han Geuk, additional, Lee, Hyun Soo, additional, and Lim, Dae-Seog, additional

Published
2019
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30. Synergistic Effect of Tolerogenic Dendritic Cells and Etanercept on a Collagen-induced Arthritis Animal Model

Author

Jung, Sang Youn, primary, Cho, Kil-Sang, additional, Jang, Doo-Rye, additional, Lee, Jun-Ho, additional, Choi, So-Yeon, additional, Byun, Sei-Hee, additional, Park, Soo-Yeoun, additional, Jung, Nam-Chul, additional, Choi, Jinjung, additional, Chung, Kwang-Hoe, additional, Jang, Jin-ah, additional, Park, Jun-Eui, additional, Lee, Hyun Soo, additional, and Lim, Dae-Seog, additional

Published
2019
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38. Infarcted Myocardium-Primed Dendritic Cells Improve Remodeling and Cardiac Function After Myocardial Infarction by Modulating the Regulatory T Cell and Macrophage Polarization

Author

Choo, Eun Ho, primary, Lee, Jun-Ho, additional, Park, Eun-Hye, additional, Park, Hyo Eun, additional, Jung, Nam-Chul, additional, Kim, Tae-Hoon, additional, Koh, Yoon-Seok, additional, Kim, Eunmin, additional, Seung, Ki-Bae, additional, Park, Cheongsoo, additional, Hong, Kwan-Soo, additional, Kang, Kwonyoon, additional, Song, Jie-Young, additional, Seo, Han Geuk, additional, Lim, Dae-Seog, additional, and Chang, Kiyuk, additional

Published
2017
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39. Asymptomatic Clostridium perfringensInhabitation in Intestine Can Cause Inflammation, Apoptosis, and Disorders in Brain

Author

Lee, Heeyoung, Lee, Soomin, Kim, Sejeong, Lee, Jeeyeon, Ha, Jimyeong, Choi, Yukyung, Oh, Hyemin, Kim, Yujin, Lee, Yewon, Lim, Dae-Seog, Kim, Saehun, Han, Young Sil, Choi, Kyoung-Hee, and Yoon, Yohan

Abstract

Clostridium perfringens(CP) is a foodborne pathogen. The bacterium can also inhabit human gut without symptoms of foodborne illness. However, the clinical symptoms of long-term inhabitation have not been known yet. Therefore, the objective of this study was to elucidate the relationship between intestinal CP and other internal organs. Phosphate-buffered saline (PBS) and CP were orally injected into 5-week-old (YOUNG) and 12-month-old C57BL6/J (ADULT) mice. Gene expression levels related to inflammation (tumor necrosis factor-α [TNF-α], interleukin [IL]-1β, and IL-6) and oxidative stress (superoxide dismutase [SOD]1, SOD2, SOD3, glutathione reductase [GSR], glutathione peroxidase [GPx]3, and catalase [CAT]) responses were evaluated in the brain, small intestine, and liver. In addition, apoptosis-related (BCL2-associated X [BAX]1and high-mobility group box-1 [HMGB1]) and brain disorder-related genes (CCAAT-enhancer-binding protein [C/EBP]-β, C/EBPδ, C/EBP homologous protein [CHOP], and amyloid precursor protein [APP]) as brain damage markers were examined. The protein expressions in the brain were also measured. Gene expression levels of inflammation and oxidative stress responses were higher (p< 0.05) in brains of CP-YOUNG and CP-ADULT mice, compared with PBS-YOUNG and PBS-ADULT, and the gene expression levels were higher (p< 0.05) in brains of CP-ADULT mice than CP-YOUNG mice. Apoptosis-related (BAX1and HMGB1) and brain disorder-related genes (C/EBPβ, C/EBPδ, CHOP,and APP) were higher (p< 0.05) in brains of CP-challenged mice, compared with PBS-challenged mice. Even oxidative stress response (GPx and SOD2), cell damage-related (HMGB1), and β-amyloid proteins were higher (p< 0.05) in brains of CP- than in PBS-challenged mice. C/EBP protein was higher (p< 0.05) in CP-YOUNG, compared with PBS-YOUNG mice. However, these clinical symptoms were not observed in small intestine and liver. These results indicate that although asymptomatic intestinal CP do not cause foodborne illness, their inhabitation may cause brain inflammation, oxidative stress, apoptosis, and cell damage, which may induce disorders, especially for the aged group.

Published
2020
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40. Activation of peroxisome proliferator‐activated receptor delta suppresses BACE1 expression by up‐regulating SOCS1 in a JAK2/STAT1‐dependent manner.

Author

Lee, Won Jin, Ham, Sun Ah, Lee, Gyeong Hee, Choi, Mi‐Jung, Yoo, Hyunjin, Paek, Kyung Shin, Lim, Dae‐Seog, Hong, Kwonho, Hwang, Jung Seok, and Seo, Han Geuk

Subjects
NUCLEAR receptors (Biochemistry), PEROXISOME proliferator-activated receptors, MICROPHTHALMIA-associated transcription factor, ALZHEIMER'S disease, CELLULAR signal transduction
Abstract

Neuronal expression of beta‐secretase 1 (BACE1) has been implicated in the progression of Alzheimer's disease. However, the mechanisms that regulate BACE1 expression are unclear. Here, we show that peroxisome proliferator‐activated receptor delta (PPARδ) decreases BACE1 expression by up‐regulating suppressor of cytokine signaling 1 (SOCS1) in SH‐SY5Y neuroblastoma cells. The activation of PPARδ by GW501516, a specific PPARδ agonist, inhibited expression of BACE1. This effect was abrogated by shRNA‐mediated knockdown of PPARδ and by treatment with the PPARδ antagonist GSK0660, indicating that PPARδ is involved in GW501516‐mediated suppression of BACE1 expression. On the other hand, GW501516‐activated PPARδ induced expression of SOCS1, which is a negative regulator of cytokine signal transduction, at the transcriptional level by binding to a PPAR response element in its promoter. This GW501516‐mediated induction of SOCS1 expression led to down‐regulation of BACE1 expression via inactivation of signal transducer and activator of transcription 1. GW501516‐activated PPARδ suppressed the generation of neurotoxic amyloid beta (Aβ) in accordance with the decrease in BACE1 expression. Taken together, these results indicate that PPARδ attenuates BACE1 expression via SOCS1‐mediated inhibition of signal transducer and activator of transcription 1 signaling, thereby suppressing BACE1‐associated generation of neurotoxic Aβ. [ABSTRACT FROM AUTHOR]

Published
2019
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46. Activation of Peroxisome Proliferator-Activated Receptor γ by Rosiglitazone Inhibits Lipopolysaccharide-Induced Release of High Mobility Group Box 1

Author

Hwang, Jung Seok, Kang, Eun Sil, Ham, Sun Ah, Yoo, Taesik, Lee, Hanna, Paek, Kyung Shin, Park, Chankyu, Kim, Jin-Hoi, Lim, Dae-Seog, and Seo, Han Geuk

Subjects
Article Subject, lcsh:Pathology, lipids (amino acids, peptides, and proteins), chemical and pharmacologic phenomena, lcsh:RB1-214
Abstract

Peroxisome proliferator-activated receptors (PPARs) are shown to modulate the pathological status of sepsis by regulating the release of high mobility group box 1 (HMGB1), a well-known late proinflammatory mediator of sepsis. Ligand-activated PPARs markedly inhibited lipopolysaccharide- (LPS) induced release of HMGB1 in RAW 264.7 cells. Among the ligands of PPAR, the effect of rosiglitazone, a specific ligand for PPARγ, was superior in the inhibition of HMGB1 release induced by LPS. This effect was observed in cells that received rosiglitazone before LPS or after LPS treatment, indicating that rosiglitazone is effective in both treatment and prevention. Ablation of PPARγ with small interfering RNA or GW9662-mediated inhibition of PPARγ abolished the effect of rosiglitazone on HMGB1 release. Furthermore, the overexpression of PPARγ markedly potentiated the inhibitory effect of rosiglitazone on HMGB1 release. In addition, rosiglitazone inhibited LPS-induced expression of Toll-like receptor 4 signal molecules, suggesting a possible mechanism by which rosiglitazone modulates HMGB1 release. Notably, the administration of rosiglitazone to mice improved survival rates in an LPS-induced animal model of endotoxemia, where reduced levels of circulating HMGB1 were demonstrated. Taken together, these results suggest that PPARs play an important role in the cellular response to inflammation by inhibiting HMGB1 release.

Published
2012

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