• The Journal of Korean Medicine
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• v.18 no.2
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• pp.43-57
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• 1997

It was claimed that the herbal medicine with the function of strengthening the body resistance exerts to enhance the immunity. And the medicine with the effect of eliminating the pathogenic factor is stated to inhibit the immune response. To evaluate the the effects of the herbal medicine on the immune response, the mice were administrated with the herbal medicine for 2 weeks. And the responses were analyzed. As the result, water extract of Radix Astragali, Fructus Psoraleae, Cortex Acanthopanacis, Semen Coicis, Herba Ecliptae, Spica Prunellae, and Radix Sophorae increased the ROI production, while Radix Tripterygia inhibited it. Phagocytic activity was increased after administration of Radix Astragal, Fructus Psoraleae, Cortex Acanthopanacis, Herba Ecliptae, Spica Prunellae and Radix Sophorae. NK cell activity was also significantly inhibited by Radix Tripterygia. Administration of Radix Astragali, Fructus Psoraleae, Cortex Acanthopanacis, Herba Ecliptae, Spica Prunellae and Semen Coicis enhanced the antibodies(hemagglutinin and hemolysin) formation and the appearance of rosette forming cells of the spleen, while Radix Sophorae and Radix Tripterygia decreased it. Radix Sophorae and Radix Tripterygia also decreased the allogenic immune response and mixed-lymphocyte reaction. And all the experimental herbs decreased contact hypersensitivity against dinitroflurobenzene. These results show Radix Astragali, Fructus Psoraleae, Spica Prunellae, Cortex Acanthopanacis, Semen Coicis and Herba Ecliptae enhanced innate immunity, humoral and cellular immune responses. However Radix Sophorae and Radix Tripterygia exert imunosuppressive action. Also these results indicate that the medicine with the action of the strengthening the body resistance enhances the immunity. And the the some of drugs belonging to the eliminating the pathogenic factor also increase the immune responses.

• IMMUNE NETWORK
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• v.20 no.3
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• pp.25.1-25.13
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• 2020

Acinetobacter baumannii is known for its multidrug antibiotic resistance. New approaches to treating drug-resistant bacterial infections are urgently required. Cathelicidin-related antimicrobial peptide (CRAMP) is a murine antimicrobial peptide that exerts diverse immune functions, including both direct bacterial cell killing and immunomodulatory effects. In this study, we sought to identify the role of CRAMP in the host immune response to multidrug-resistant Acinetobacter baumannii. Wild-type (WT) and CRAMP knockout mice were infected intranasally with the bacteria. CRAMP^-/- mice exhibited increased bacterial colony-forming units (CFUs) in bronchoalveolar lavage (BAL) fluid after A. baumannii infection compared to WT mice. The loss of CRAMP expression resulted in a significant decrease in the recruitment of immune cells, primarily neutrophils. The levels of IL-6 and CXCL1 were lower, whereas the levels of IL-10 were significantly higher in the BAL fluid of CRAMP^-/- mice compared to WT mice 1 day after infection. In an in vitro assay using thioglycollate-induced peritoneal neutrophils, the ability of bacterial phagocytosis and killing was impaired in CRAMP^-/- neutrophils compared to the WT cells. CRAMP was also essential for the production of cytokines and chemokines in response to A. baumannii in neutrophils. In addition, the A. baumannii-induced inhibitor of κB-α degradation and phosphorylation of p38 MAPK were impaired in CRAMP^-/- neutrophils, whereas ERK and JNK phosphorylation was upregulated. Our results indicate that CRAMP plays an important role in the host defense against pulmonary infection with A. baumannii by promoting the antibacterial activity of neutrophils and regulating the innate immune responses.

• Journal of Microbiology and Biotechnology
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• v.27 no.10
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• pp.1727-1735
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• 2017

Hepatitis E virus (HEV) infections cause epidemic or sporadic acute hepatitis, which are mostly self-limiting. However, viral infection in immunocompromised patients and pregnant women may result in serious consequences, such as chronic hepatitis and liver damage, mortality of the latter of which reaches up to 20-30%. Type I interferon (IFN)-induced antiviral immunity is known to be the first-line defense against virus infection. Upon HEV infection in the cell, the virus genome is recognized by pathogen recognition receptors, leading to rapid activation of intracellular signaling cascades. Expression of type I IFN triggers induction of a barrage of IFN-stimulated genes, helping the cells cope with viral infection. Interestingly, some of the HEV-encoded genes seem to be involved in disrupting signaling cascades for antiviral immune responses, and thus crippling cytokine/chemokine production. Antagonistic mechanisms of type I IFN responses by HEV have only recently begun to emerge, and in this review, we summarize known HEV evasion strategies and compare them with those of other hepatitis viruses.

• Journal of Ginseng Research
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• v.32 no.1
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• pp.67-72
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• 2008

for 4 h, tumoricidal activity was significantly increased. However, NSRG had effects on tumoricidal activity of macrophages at low concentration (1 ug/ml), which was not related to the production of nitric oxide. The mitogen response of lymphocytes to LPS and ConA in the spleen did not show significant differences between the control and NSRG-treated cells, whereas LPS-induced blastogenesis was slightly increased at 100 ${\mu}g/ml$ (p < 0.05). These results suggest that NSRG has differential effects on innate immune response and could be useful as immunotherapy for cancer treatment.

• International Journal of Oral Biology
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• v.42 no.3
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• pp.85-90
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• 2017

Mitochondria participate in various intracellular metabolic pathways such as generating intracellular ATP, synthesizing several essential molecules, regulating calcium homeostasis, and producing the cell's reactive oxygen species (ROS). Emerging studies have demonstrated newly discovered roles of mitochondria, which participate in the regulation of innate immune responses by modulating NLRP3 inflammasomes. Here, we review the recently proposed pathways to be involved in mitochondria-mediated regulation of inflammasome activation and inflammation: 1) mitochondrial ROS, 2) calcium mobilization, 3) nicotinamide adenine dinucleotide ($NAD^+$) reduction, 4) cardiolipin, 5) mitofusin, 6) mitochondrial DNA, 7) mitochondrial antiviral signaling protein. Furthermore, we highlight the significance of mitophagy as a negative regulator of mitochondrial damage and NLRP3 inflammasome activation, as potentially helpful therapeutic approaches which could potentially address uncontrolled inflammation.

• Animal cells and systems
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• v.13 no.1
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• pp.1-8
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• 2009

Toll-like receptor (TLR) family proteins, type I transmembrane proteins, play a central role in human innate immune response by recognizing common structural patterns in diverse molecules from bacteria, viruses and fungi. Recently four structures of the TLR and ligand complexes have been determined by high resolution x-ray crystallographic technique. In this review we summarize reported structures of TLRs and their proposed activation mechanisms. The structures demonstrate that binding of agonistic ligands to the extracellular domains of TLRs induces homo- or heterodimerization of the receptors. Dimerization of the TLR extracellular domains brings their two C-termini into close proximity. This suggests a plausible mechanism of TLR activation: ligand induces dimerization of the extracellular domains, which enforces juxtaposition of intracellular signaling domains for recruitment of intracellular adaptor proteins for signal initiation.

• Journal of Microbiology and Biotechnology
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• v.29 no.10
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• pp.1506-1521
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• 2019

Tuberculosis, which is caused by Mycobacterium tuberculosis (Mtb), is among the most pressing worldwide problems. Mtb uniquely interacts with innate immune cells through various pattern recognition receptors. These interactions initiate several inflammatory pathways that play essential roles in controlling Mtb pathogenesis. Although the TLR signaling pathways have essential roles in numerous host's immune defense responses, the role of TLR signaling in the response to Mtb infection is still unclear. This review presents discussions on host-Mtb interactions in terms of Mtb-mediated TLR signaling. In addition, we highlight recent discoveries pertaining to these pathways that may help in new immunotherapeutic opportunities.

• Proceedings of the Microbiological Society of Korea Conference
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• 2008.05a
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• pp.70-70
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• 2008

• IMMUNE NETWORK
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• v.3 no.4
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• pp.261-267
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• 2003

The periodontal diseases are infections caused by bacteria in oral biofilm, a gelatinous mat commonly called dental plaque, which is a complex microbial community that forms and adhere to tooth surfaces. Host immune-pathogen interaction in periodontal disease appears to be a complex process, which is regulated not only by the acquired immunity to deal with ever-growing and -invading microorganisms in periodontal pockets, but also by genetic and/or environmental factors. However, our understanding of the pathogenesis in human periodontal diseases is limited by the lack of specific and sensitive tools or models to study the complex microbial challenges and their interactions with the host's immune system. Recent advances in cellular and molecular biology research have demonstrated the importance of the acquired immune system in fighting the virulent periodontal pathogens and in protecting the host from developing further devastating conditions in periodontal infections. The use of genetic knockout and immunodeficient mouse strains has shown that the acquired immune response, in particular, $CD4^+$ T-cells plays a pivotal role in controlling the ongoing infection, the immune/inflammatory responses, and the subsequent host's tissue destruction.

• Journal of Ginseng Research
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• v.36 no.4
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• pp.354-368
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• 2012

Thousands of literatures have described the diverse role of ginseng in physiological processes such as cancer, neurodegenera tive disorders, insulin resistance, and hypertension. In particular, ginseng has been extensively reported to maintain homeostasis of the immune system and to enhance resistance to illness or microbial attacks through the regulation of immune system. Immune system comprises of different types of cells fulfilling their own specialized functions, and each type of the immune cells is differentially influenced and may be simultaneously controlled by ginseng treatment. This review summarizes the current knowledge on the effects of ginseng on immune system. We discuss how ginseng regulates each type of immune cells including macrophages, natural killer cells, dendritic cells, T cells, and B cells. We also describe how ginseng exhibits beneficial effects on controlling inflammatory diseases and microbial infections.