• Genomics & Informatics
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• v.3 no.3
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• pp.63-67
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• 2005

Adaptive responses to diverse microbial pathogens might be limited in relatively few types. Host cell responses to pathogens are believed to be patterned or stereotyped along with species or class. We tried to compose the host response to Mycoplasma in terms of cellular gene expression. Although gene expression profile of two host HeLa and 293 cells were quite different each other, 30 genes were differentially expressed by mycoplasma infection in both of HeLa and 293 cells. Six of them (PR48, MADH4, MKPX, CRK, RBM7, NEK3) were related to cell cycle or proliferation. Another category of genes like IL1 HY1, KLRF1, TNFSF14, GBP1 were host defense to elicit immune responses. With this set of genes, we establish the prediction model for mycoplasma contamination.

• The Korean Journal of Physiology and Pharmacology
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• v.16 no.5
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• pp.349-353
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• 2012

Activated T cells express inhibitory receptors such as CTLA-4 that can downregulate immune responses. Blockade of or genetic deficiency in CTLA-4 can result in autoimmunity. Therefore, strategies to increase the inhibitory function of CTLA-4 may be attractive in settings of undesirable T cell responses such as autoimmunity or transplant rejection. We have tested the hypothesis that transgenic constitutive expression of CTLA-4 can further attenuate immune responses when compared with normal inducible expression. Our results indicate that transgenic expression of CTLA-4 in mouse T cells (CTLA-4-Tg T cells) results in reduced cell cycle progression and increased apoptosis of TCR-stimulated T cells. CTLA-4-Tg T cells display reduced T cell proliferation in an in vivo model of graft versus host disease (GVHD). These results further our understanding of how CTLA-4 can be manipulated to inhibit immune responses and may help development of new therapeutic strategies for clinical settings of autoimmunity and transplantation.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.151-152
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• 2002

Bacterial infection is a very complex process in which both pathogenic microorganisms and host cells play crucial roles, and it is the outcome of interactions between the two participants. To elucidate the bacterial pathogenesis mechanisms, therefore, it is essential to understand the cellular and systemic responses of the host as well as the virulence factors of the pathogen. Infection of a host by pathogenic bacteria causes drastic changes in the physiology of host cells, leading to activation of a program of various gene expression. (omitted)

• The Plant Pathology Journal
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• v.20 no.1
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• pp.22-29
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• 2004

Many important horticultural and field crops are susceptible to virus infections or may possess a degree of resistance to some viruses, but become infected by others. Plant viruses enter cells through the presence of wounds, and replicate intracellularly small genomes that encode genes required for replication, cell-to-cell movement and encapsidation. There are numerous evidences from specific virus-host interactions to require the involvement of host factors and steps during viral replication cycle. However, viruses should deal with host defense responses either by general or specific mechanisms, targeting viral components or genome itself. On the other hand, the host plants have also adapted to defend themselves against viral attack by operating different lines of resistance responses. The defense-related interactions provide new insights into the complex molecular strategies for hosts for defense and counter-defense employed by viruses.

• BMB Reports
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• v.42 no.12
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• pp.776-787
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• 2009

T helper (Th) 17 cells have recently been described as a third subset of T helper cells, and have provided new insights into the mechanisms that are important in the development of autoimmune diseases and the immune responses that are essential for effective antimicrobial host defense. Both protective and harmful effects of Th17 responses during infection have been described. In general, Th17 responses are critical for mucosal and epithelial host defense against extracellular bacteria and fungi. However, recent studies have reported that Th17 responses can also contribute to viral persistence and chronic inflammation associated with parasitic infection. It has become evident that the type of microorganisms and the setting in which they trigger the Th17 response determines the outcome of the delicate balancethat exists between Th17 induced protection and immunopathogenesis.

• Korean Journal of Poultry Science
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• v.35 no.3
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• pp.225-240
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• 2008

Marek's disease virus(MDV) is a highly cell-associated, lymphotropic $\alpha$-herpesvirus that causes paralysis and neoplastic disease in chickens. The disease has been controlled by vaccination which was provided the first evidence for a malignant cancer being controlled by an antiviral vaccine. Marek's disease pathogenesis is complex, involving cytolytic and latent infection of lymphoid cells and oncogenic transformation of $CD4^+$ T cells in susceptible chickens. MDV targets a number of different cell types during its life cycle. Lymphocytes play an essential role, although within them virus production is restricted and only virion are produced. Innate and adaptive immune responses develop in response to infection, but infection of lymphocytes results in immunosuppressive effects. Hence in MDV-infected birds, MDV makes its host more vulnerable to tumour development as well as to other pathogens. All chickens are susceptible to MDV infection, and vaccination is essential to protect the susceptible host from developing clinical disease. Nevertheless, MDV infects and replicates in vaccinated chickens, with the challenge virus being shed from the feather-follicle epithelium. The outcome of infection with MDV depends on a complex interplay of factors involving the MDV pathotype and the host genotype. Host factors that influence the course of MD are predominantly the responses of the innate and adaptive immune systems, and these are modulated by: age at infection and maturity of the immune system; vaccination status; the sex of the host; and various physiological factors.

• IMMUNE NETWORK
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• v.14 no.2
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• pp.100-106
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• 2014

Infection with invasive Shigella species results in intestinal inflammation in humans but no symptoms in adult mice. To investigate why adult mice are resistant to invasive shigellae, 6~8-week-old mice were infected orally with S. flexneri 5a. Shigellae successfully colonized the small and large intestines. Mild cell death was seen but no inflammation. The infected bacteria were cleared 24 hours later. Microarray analysis of infected intestinal tissue showed that several genes that are involved with the sphingosine-1-phosphate (S1P) signaling pathway, a lipid mediator which mediates immune responses, were altered significantly. Shigella infection of a human intestinal cell line modulated host S1P-related genes to reduce S1P levels. In addition, co-administration of S1P with shigellae could induce inflammatory responses in the gut. Here we propose that Shigella species have evasion mechanisms that dampen host inflammatory responses by lowering host S1P levels in the gut of adult mice.

• The Plant Pathology Journal
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• v.34 no.2
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• pp.113-120
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• 2018

Chlorella, one single-cell green algae organism that lives autotrophically by photosynthesis, can directly suppress some plant diseases. The objective of this study was to determine whether pre-spraying with Chlorella fusca suspension could induce systemic acquired resistance (SAR) in cucumber plants against anthracnose caused by Colletotrichum orbiculare. In order to illustrate SAR induced by algae, infection structures in host cells were observed under a transmission electron microscope (TEM). Cytological changes as defense responses of host mesophyll cells such as accumulation of vesicles, formation of sheath around penetration hyphae, and thickness of cell wells adjoining with intracellular hyphae were demonstrated in cucumber leaves. Similar defense responses were also found in the plant pre-treated with DL-3-aminobutyric acid, another SAR priming agent. Images showed that defense response of host cells was scarcely observed in untreated leaf tissues. These cytological observations suggest that C. fusca could induce SAR against anthracnose in cucumber plants by activating defense responses of host cells.

• Molecules and Cells
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• v.27 no.1
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• pp.5-14
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• 2009

The availability of effective vaccines has had the most profound positive effect on improving the quality of public health by preventing infectious diseases. Despite many successful vaccines, there are still old and new emerging pathogens against which there is no vaccine available. A better understanding of how vaccines work for providing protection will help to improve current vaccines as well as to develop effective vaccines against pathogens for which we do not have a proper means to control. Recent studies have focused on innate immunity as the first line of host defense and its role in inducing adaptive immunity; such studies have been an intense area of research, which will reveal the immunological mechanisms how vaccines work for protection. Toll-like receptors (TLRs), a family of receptors for pathogen-associated molecular patterns on cells of the innate immune system, play a critical role in detecting and responding to microbial infections. Importantly, the innate immune system modulates the quantity and quality of long-term T and B cell memory and protective immune responses to pathogens. Limited studies suggest that vaccines which mimic natural infection and/or the structure of pathogens seem to be effective in inducing long-term protective immunity. A better understanding of the similarities and differences of the molecular and cellular events in host responses to vaccination and pathogen infection would enable the rationale for design of novel preventive measures against many challenging pathogens.

• Journal of Plant Biotechnology
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• v.36 no.3
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• pp.244-254
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• 2009

The hypersensitive reaction (HR) is the most common plant defense reaction against pathogens. HR is produced during both host- and nonhost-incompatible interactions. Several reports suggest that similarities exist between host and nonhost resistances. We assayed the pattern of generation of reactive oxygen species (ROS) and scavenging enzyme activities during nonhost pathogen-plant interactions (Xanthomonas campestris pv. campestris/Capsicum annuum L.) and incompatible host pathogen-plant interactions (Xanthomonas campestris pv. vesicatoria race1/Capsicum annuum L.). Both ${O_2}^-\;and\;H_2O_2 $ accumulated much faster during nonhost resistance when compared to the host resistance. The scavenging enzyme activities of superoxide dismutase (SOD), catalase (CAT) and peroxidase (POX) were also different during the host- and nonhost-incompatible interactions. CAT activity was much higher during nonhost resistance, and several new isozymes of SOD and POX were detected during nonhost resistance when compared to the host resistance. Lipoxygenase (LOX) activity was higher in host resistance than nonhost resistance during the early stages of infection. Interestingly, the nitric oxide (NO) radical accumulated equal amounts during both host and nonhost resistance at early stages of infection. Further studies are needed to determine the specific pathways underlying these differences between host and nonhost resistance responses.