• IMMUNE NETWORK
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• v.4 no.2
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• pp.73-80
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• 2004

Viruses are obligate intracellular parasites which cause infection by invading and replicating within cells. The immune system has mechanisms which can attack the virus in extracellular and intracellular phase of life cycle, and which involve both non-specific and specific effectors. The survival of viruses depends on the survival of their hosts, and therefore the immune system and viruses have evolved together. Immune responses to viral infection may be variable depending on the site of infection, the mechanism of cell-to-cell spread of virus, physiology of the host, host genetic variation, and environmental condition. Viral infection of cells directly stimulates the production of interferons and they induce antiviral state in the surrounding cells. Complement system is also involved in the elimination of viruses and establishes the first line of defence with other non-specific immunity. During the course of viral infection, antibody is most effective at an early stage, especially before the virus enters its target cells. The virus- specific cytotoxic T lymphocytes are the principal effector cells in clearing established viral infections. But many viruses have resistant mechanism to host immune responses in every step of viral infection to cells. Some viruses have immune evasion mechanism and establish latency or persistency indefinitely. Furthermore antibodies to some viruses can enhance the disease by the second infection. Immune responses to viral infection are very different from those to bacterial infection.

• IMMUNE NETWORK
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• v.2 no.2
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• pp.65-71
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• 2002

The immunological mechanism of the responses to ultraviolet (UV) B radiation in mouse models were investigated by the suppression of contact hypersensitivity (CHS) and delayed type hypersensitivity (DTH), and susceptibility to infection. However, there are some differences in immune suppression according to the different models as well as the irradiation protocols. Therefore, this review focused on the differences in the suppressive effects on CHS and DTH, and susceptibility to infection in relation to the different in vivo models. Recent advances in cytokine knockout mice experiments have the reexamination of the role of the critical cytokines in UVB-induced immune suppression, which was investigated previously by blocking antibodies. The characteristics of the suppressor cells responsible for UVB-induced tolerance were determined. The subcellular mechanism of UVB-induced immune suppression was also explained by the induction of apoptotic cells through the Fas and Fas-ligand interaction. The phagocytosis of the apoptotic cells is believed to induce the production of the immune suppressive cytokine like interleukin-10 by macrophages. Therefore, the therapeutic UVB response to a skin disease, such as psoriasis, by the depletion of infiltrating T cells could be considered in the extension line of apoptosis and immune suppression.

• Food Science of Animal Resources
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• v.30 no.4
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• pp.568-574
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• 2010

This study introduced a chick embryos’ infection model to elucidate the pathogenesis mechanism of Pseudomonas aeruginosa, which causes serious diseases in human after ingestion of P. aeruginosa-contaminated animal originated foods. The embryonic chick model is able to give a rapid and relatively inexpensive method to assess bacterial pathogenicity compared to embryos of other vertebrates. Embryos were infected with P. aeruginosa and elastase-deficient P. aeruginosa. After infection with P. aeruginosa cells, total bacterial cell numbers and gelatinase activities in the embryos were compared. Thereafter, precartilage condensation and chondrogenesis were assessed by peanut agglutinin (PNA) binding on day 3 and by Alcian blue staining for sulfated proteoglycans on day 5, respectively. P. aeruginosa significantly increased in embryos, resulting in abnormal limb development, whereas P. aeruginosa defective in elastase activity partly impaired proliferation. In addition, P. aeruginosa-infected chick embryos significantly stimulated the production of matrix metalloproteinases. Several analyses showed that elevated proteases suppressed the proliferation and survival of chondrogenic cells. The results show that this infection model was a useful assay to determine the virulence mechanism of P. aeruginosa in human after intake of microbiologically contaminated foods.

• Biomedical Science Letters
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• v.13 no.4
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• pp.325-332
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• 2007

Cell-mediated immune response (CMI) is a major immune protective mechanism against tuberculosis (TB) infection. Among several components involved in CMI, recent studies suggest that CD8+ T cells are important in controlling TB infection. In our previous report, we defined four Mycobacterium tuberculosis (MTB) derived epiotpe peptides specific for HLA-A*0201-restricted CD8+ T cells. These four peptides are $PstAl_{75-83}$, $ThyA_{30-38}$, $RpoB_{127-135}$ and $85B_{15-23}$. In this study, these epitope peptides specific CD8+ T cell responses in tuberculous pleurisy were investigated using ex vivo $IFN-\gamma$ elispot assay and intracellular $IFN-\gamma$ staining method. As a result, we observed these epitope peptide specific CD8+ T cell responses are induced in all three patients with tuberculous pleurisy suggesting that CD8+ T cells are involved in protective immune mechanism against MTB infection in tuberculous pleurisy. However, the CMI to mitogens and MTB antigens from pleural fluids of patients with tuberculous pleurisy does not seem to correlate with that from peripheral blood, although the sample size is too small to make any conclusion. In sum, the MHC I restricted CD8+ T cell responses seem to be induced efficiently in the pleural fluids, at the site of TB infection, in which the CMI is actively induced. In addition, these experiments suggest that MHC I restricted CD8+ T cell mediated immune responses are also involved in protective mechanism against MTB infection in extra-pulmonary TB.

• Journal of Microbiology and Biotechnology
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• v.32 no.7
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• pp.844-854
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• 2022

Helicobacter pylori, a group 1 carcinogen, colonizes the stomach and affects the development of stomach diseases. Progranulin (PGRN) is an autocrine growth factor that regulates multiple cellular processes and plays a tumorigenic role in many tissues. Nevertheless, the mechanism of action of PGRN in gastric cancer caused by H. pylori infection remains unclear. Here, we investigated the role of PGRN in cell cycle progression and the cell proliferation induced by H. pylori infection. We found that the increased PGRN was positively associated with CDK4 expression in gastric cancer tissue. PGRN was upregulated by H. pylori infection, thereby promoting cell proliferation, and that enhanced level of proliferation was reduced by PGRN inhibitor. CDK4, a target gene of PGRN, is a cyclin-dependent kinase that binds to cyclin D to promote cell cycle progression, which was upregulated by H. pylori infection. We also showed that knockdown of CDK4 reduced the higher cell cycle progression caused by upregulated PGRN. Moreover, when the PI3K/Akt signaling pathway (which is promoted by PGRN) was blocked, the upregulation of CDK4 mediated by PGRN was reduced. These results reveal the potential mechanism by which PGRN plays a major role through CDK4 in the pathological mechanism of H. pylori infection.

• BMB Reports
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• v.53 no.9
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• pp.449-452
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• 2020

The inner ear is a complex and delicate structure composed of the cochlea and the vestibular system. To maintain normal auditory function, strict homeostasis of the inner ear is needed. A proper immune response against infection, thus, is crucial. Also, since excessive immune reaction can easily damage the normal architecture within the inner ear, the immune response should be fine regulated. The exact mechanism how the inner ear's immune response, specifically the innate immunity, is regulated was unknown. Recently, we reported a protein selectively localized in the inner ear during bacterial infection, named cochlin, as a possible mediator of such regulation. In this review, the immunological function of cochlin and the mechanism behind its role within inner ear immunity is summarized. Cochlin regulates innate immunity by physically entrapping pathogens within scala tympani and recruiting innate immune cells. Such mechanism enables efficient removal of pathogen while preserving the normal inner ear structure from inflammatory damage.

• Proceedings of the Microbiological Society of Korea Conference
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• 2001.11a
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• pp.97-101
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• 2001

The fusion between viral envelope and target cell membrane is a central step of viral infection, and the fusion proteins located at viral envelope mediate such process. Gp41 of HIV is one of the fusion proteins whose structure and mechanism of membrane fusion had been extensively studied. Functionally important motives of gp41 are the N-terminus fusion peptide, the coiled-coil and the membrane proximal C-peptide regions. The role of these regions during the fusion process had been thoroughly examined. Specially, insertion of the fusion peptide into membrane and conformational change of the coiled-coil and C-peptide regions are assumed to be critical for the fusion mechanism. In addition, the coiled-coil region has been shown to interact with membrane, and the C-peptide region regulates the interaction in a dose dependent manner. Furthermore, fusion defective mutations of the coiled-coil region dramatically changed its binding affinity to membrane. These results suggested that the membrane binding property of the coiled-coil region is important for the fusion activity of gp41, and such property could be modulated by the interaction with the C-peptide region.

• Proceedings of the Microbiological Society of Korea Conference
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• 2008.05a
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• pp.37-37
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• 2008

• Journal of the Institute of Electronics Engineers of Korea TC
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• v.43 no.7 s.349
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• pp.24-31
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• 2006

Traditional security mechanisms do not work well in the sensor network area due to the sensor's resource constraints. Therefore security issues are challenging problems on realization of the sensor network. Among them, the key establishment is one of the most important and challenging security primitives which establish initial associations between two nodes for secure communications. Recently, R. Anderson et al. proposed one of the promising key establishment schemes for commodity sensor network called Key Infection. However, key infection has an intrinsic vulnerability that there are some areas where adversaries can eavesdrop on the transferred key information at initial key establishment time. Therefore, in this paper, we propose a security-enhanced key establishment scheme for key infection by suggesting a mechanism which effectively reduces the vulnerable areas. The proposed security mechanism uses other neighbor nodes' additional key information to establish pair-wise key at the initial key establishment time. By using the additional key information, we can establish security-enhanced key establishment, since the vulnerable area is decreased than the key infection's. We also evaluate our scheme by comparing it with key infection using logical and mathematical analysis.

• Korean Journal of Soil Science and Fertilizer
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• v.45 no.4
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• pp.622-627
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• 2012

The processes to determine the composition, dynamics, and activity of infection mechanisms by the rhizosphere microflora have attracted the interest of scientists from multiple disciplines although considerable progress of the infection pathways and plant-pathogen interactions by soil borne fungal pathogens have been made. Soilborne pathogens are confined within a three-dimensional matrix of mineral soil particles, pores, organic matter in various stages of decomposition and a biological component. Among the physical and chemical properties of soils soil texture and matric water potential may be the two most important factors that determine spread exudates by soil borne fungal pathogens, based on the size of the soil pores. Pathogenic invasion of plant roots involves complex molecular mechanisms which occur in the diffuse interface between the root and the soil created by root exudates. The initial infection by soilborne pathogens can be caused by enzymes which breakdown cell wall layers to penetrate the plant cell wall for the fungus. However, the fate and mobility of the exudates are less well understood. Therefore, it needs to develop methods to control disease caused by enzymes produced by the soilborne pathogens by verifying many other possible pathways and mechanisms of infection processes occurring in soils.