Tae Il Kim
Yonsei University · Medicine
About the Lab
Professor Tae Il Kim's research lab specializes in translational immunology and neurovascular physiology, with a focus on innate immune sensing mechanisms—particularly Toll-like receptor 9 and DExD/H-box helicases—in dendritic cells and their roles in type I interferon responses. The lab also investigates clinical applications in gastrointestinal diseases, such as intestinal Behçet’s disease, and explores the impact of metabolic modulators like metformin on colorectal cancer outcomes in diabetic patients. Additionally, the lab employs high-field MRI techniques to quantify cerebral blood volume dynamics and neurovascular coupling in animal models, advancing functional MRI methodology. These interdisciplinary efforts bridge molecular immunology, clinical gastroenterology, and neuroimaging.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15Toll-like receptor 9 (TLR9) senses microbial DNA and triggers type I IFN responses in plasmacytoid dendritic cells (pDCs). Previous studies suggest the presence of myeloid differentiation primary response gene 88 (MyD88)-dependent DNA sensors other than TLR9 in pDCs. Using MS, we investigated C-phosphate-G (CpG)-binding proteins from human pDCs, pDC-cell lines, and interferon regulatory factor 7 (IRF7)-expressing B-cell lines. CpG-A selectively bound the aspartate-glutamate-any amino acid-aspart
Nine factors have been found to be associated with IPPB and polypectomy should be undertaken with caution under these conditions.
Metformin use has been associated with decreased cancer risk and mortality. However, the effects of metformin on clinical outcomes of colorectal cancer (CRC) are not defined. This study aimed to evaluate the association between metformin use and mortality of CRC in diabetic patients. We identified 595 patients who were diagnosed both CRC and diabetes mellitus. Patients were compared by two groups; 258 diabetic patients taking metformin and 337 diabetic patients not taking metformin. Patient's de
Quantifying both arterial cerebral blood volume (CBV(a)) changes and total cerebral blood volume (CBV(t)) changes during neural activation can provide critical information about vascular control mechanisms, and help to identify the origins of neurovascular responses in conventional blood oxygenation level dependent (BOLD) magnetic resonance imaging (MRI). Cerebral blood flow (CBF), CBV(a), and CBV(t) were quantified by MRI at 9.4 T in isoflurane-anesthetized rats during 15-s duration forepaw sti
OBJECTIVES: It is difficult to diagnose intestinal Behçet's disease (BD) due to various extraintestinal manifestations emerging at different time points in the disease course and a lack of reliable diagnostic criteria. We conducted this study to develop and validate novel diagnostic criteria for intestinal BD. METHODS: Experts from three universities generated the preliminary diagnostic criteria for intestinal BD, and a consensus was reached using a modified Delphi method with 13 gastroenterolog
Determination of compartment-specific cerebral blood volume (CBV) changes is important for understanding neurovascular physiology and quantifying blood oxygenation level-dependent (BOLD) functional magnetic resonance imaging (fMRI). In isoflurane-anesthetized cats, we measured the spatiotemporal responses of arterial CBV (CBV(a)) and total CBV (CBV(t)) induced by a 40-second visual stimulation, using magnetization transfer (MT)-varied BOLD and contrast-agent fMRI techniques at 9.4 T. To determin
Genotoxic stress triggers signal transduction pathways that mediate either the protection or apoptosis of affected cells. The interferon regulatory factors (IRFs) are involved in a wide range of host defense mechanisms against environmental stresses. Treatment with DNA-damaging agents, including doxorubicin and UV radiation, caused phosphorylation of the IRF3 transcription factor. Phosphorylation of IRF3 induced its interaction with the transcriptional co-activator cAMP-response element binding
Metformin has been known to suppress cancer stem cells (CSCs) in some cancers. However, the differential effects of metformin on CSCs and their mechanisms have not been reported. Herein, metformin induced pAMPK activation and pS6 suppression in metformin-sensitive (HT29) cells, but not in metformin-resistant (SW620) cells. The oxygen consumption rate was higher in HT29 cells than in SW620 cells and showed a prominent decrease after metformin treatment in HT29 cells. In glutamine-depleted medium,
Cancer stem cells (CSCs) play a pivotal role in cancer relapse or metastasis. We investigated the CSC-suppressing effect of nonsteroidal anti-inflammatory drugs (NSAIDs) and the relevant mechanisms in colorectal cancer. We measured the effect of NSAIDs on CSC populations in Caco-2 or SW620 cells using colosphere formation and flow cytometric analysis of PROM1 (CD133)(+) CD44(+) cells after indomethacin treatment with/without prostaglandin E2 (PGE2) or peroxisome proliferator-activated receptor γ
Drosophila protects itself from infection by microbial organisms by means of its pivotal defense, the so-called innate immunity system. This is its sole defense as it lacks an adaptive immunity system such as is found in mammals. The strong conservation of innate immunity systems in organisms from Drosophila to mammals, and the ease with which Drosophila can be manipulated genetically, makes this fly a good model system for investigating the mechanisms of virulence of a number of medically impor
Metformin is a well-known AMPK (AMP-activated protein kinase) activator that suppresses cancer stem cells (CSCs) in some cancers. However, the mechanisms of the CSC-suppressing effects of metformin are not yet well understood. In this study, we investigated the CSC-suppressive effect of metformin via the mevalonate (MVA) pathway in colorectal cancer (CRC). Two colorectal cancer cell lines, HT29 and DLD-1 cells, were treated with metformin, mevalonate, or a combination of the two. We measured CSC
Research Areas
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