• Journal of Preventive Medicine and Public Health
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• v.35 no.4
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• pp.287-294
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• 2002

Objectives : To examine whether cumulative chronic stress influences the immune status, and to verify the effect of social support on the relationship between these two dimensions in male manufacturing workers. Methods : A total of 39 workers were recruited for this study. A structured-questionnaire was used to assess general characteristics, job characteristics (work demand and decision latitude), psychosocial distress, and social support. The serum levels of CD4 and CD8 were measured as immune markers, and were collected between 8:00 and 10:00am in order to standardize the markers. Nonparametric statistics were used to estimate the differences between job characteristics and the immune markers. Results : General characteristics, and health-related behaviors, were not associated with CD4, CD8 or CD4/CD8. No relationships were found between job characteristics and the mean levels of immune reactivity. These results were consistent, even after controlling for social support. Social support failed to modify the relationship toward work demand, decision latitude or psychosocial distress to CD4, CD8, and CD4/CD8. Conclusion : Cumulative chronic life stress might not influence the immune status, and the effects of social support on the immune function under chronic stress, may not play a crucial role in modifying the relationships. This implication supports that the effect of stress on the immune function may be determined by the characteristics of that stress. further research should effectively considers the type, magnitude and timing of a stress event, and modifiable factors, such as personality traits, coping style, and hormone excretion levels, on the alteration of immune status.

• Proceedings of the Korean Institute of Intelligent Systems Conference
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• 1997.10a
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• pp.267-270
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• 1997

As an approach to develope a control system with robustness in changing control environment conditions, this paper will propose a robot manipulator control system using multilayer neural network and immune algorithm. The proposed immune algorithm which has the characteristics of immune system such as distributed and anomaly detection, probabilistic detection, learning and memory, consists of the innate immune algorithm and the adaptive immune algorithm. We will demonstrate the effectiveness of the proposed control system with simulations of a 2-link robot manipulator.

• Journal of Korean Port Research
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• v.13 no.2
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• pp.389-398
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• 1999

In the biological immunity, the immune system of organisms regulates the antibody and T-cells to protect the attack from the foreign materials which are virus, germ cell, and other antigens, and supports their stable state. It has similar characteristics that has the adaptation and robustness to overcome disturbances and to control the plant of engineering application. In this paper, we build a model of the T-cell regulated immune response mechanism. We have also designed an immune response controller(IRC) focusing on the T-cell regulated immune response of the biological immune system that include both a help part to control the response and a suppress part to adjust system stabilization effect. We show some computer simulation to control the vibration of building structure system with strong wind forces excitation also demonstrate the efficiency of the proposed controller for applying a practical system even with existing nonlinear terms.

• 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.

• IMMUNE NETWORK
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• v.20 no.6
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• pp.44.1-44.19
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• 2020

The human body is continuously threatened by pathogens, and the immune system must maintain a balance between fighting infection and becoming over-activated. Mucosal surfaces cover several anatomically diverse organs throughout the body, such as the respiratory and gastrointestinal tracts, and are directly exposed to the external environment. Various pathogens invade the body through mucosal surfaces, making the mucosa the frontline of immune defense. The immune systems of various mucosal tissues display distinctive features that reflect the tissues' anatomical and functional characteristics. This review discusses the cellular components that constitute the respiratory and gastrointestinal tracts; in particular, it highlights the complex interactions between epithelial and immune cells to induce Ag-specific immune responses in the lung and gut. This information on mucosal immunity may facilitate understanding of the defense mechanisms against infectious agents that invade mucosal surfaces, such as severe acute respiratory syndrome coronavirus 2, and provide insight into effective vaccine development.

• Proceedings of the IEEK Conference
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• 1998.06a
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• pp.441-444
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• 1998

This paper is concerned with researching latch-up immune CMOS structure was performed. By the simulation results, the connecting layer had more effect than the buried layer to latch-up immune. When the connecting layer was the dose 1*10$^{14}$ /cm$^{2}$ and the energy 500KeV, the trigger current was more 0.6mA/.mu.m and the trigger voltage was 6V. The more the connecting layer dose was lower, the more the latch-up immune characteristics was butter.

• Proceedings of the KIEE Conference
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• 2005.05a
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• pp.72-74
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• 2005

In this paper, we propose an adaptive PID controller using a cell-mediated immune response to improve a PID control performance. The proposed controller is based on the specific immune response of the biological immune system that is cell-mediated immunity. The immune system of organisms in the real body regulates the antibody and the T-cells to protect an attack from the foreign materials like virus, germ cells, and other antigens. It has similar characteristics that are the adaptation and robustness to overcome disturbances and to control the plant of engineering application. We first build a model of the T-cell regulated immune response mechanism and then designed an I-PID controller focusing on the T-cell regulated immune response of the biological immune system. We apply the proposed methodology to building structures to mitigate vibrations due to strong winds for evaluation of control performances. Through computer simulations, system responses are illustrated and additionally compared to traditional control approaches.

• IMMUNE NETWORK
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• v.12 no.3
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• pp.71-83
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• 2012

T cell activation and function require physical contact with antigen presenting cells at a specialized junctional structure known as the immunological synapse. Once formed, the immunological synapse leads to sustained T cell receptor-mediated signalling and stabilized adhesion. High resolution microscopy indeed had a great impact in understanding the function and dynamic structure of immunological synapse. Trends of recent research are now moving towards understanding the mechanical part of immune system, expanding our knowledge in mechanosensitivity, force generation, and biophysics of cell-cell interaction. Actin cytoskeleton plays inevitable role in adaptive immune system, allowing it to bear dynamic and precise characteristics at the same time. The regulation of mechanical engine seems very complicated and overlapping, but it enables cells to be very sensitive to external signals such as surface rigidity. In this review, we focus on actin regulators and how immune cells regulate dynamic actin rearrangement process to drive the formation of immunological synapse.

• IMMUNE NETWORK
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• v.20 no.1
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• pp.9.1-9.21
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• 2020

Immune checkpoint inhibitors (ICIs) have been changing the paradigm of cancer treatment. However, immune-related adverse effects (irAEs) have also increased with the exponential increase in the use of ICIs. ICIs can break up the immunologic homeostasis and reduce T-cell tolerance. Therefore, inhibition of immune checkpoint can lead to the activation of autoreactive T-cells, resulting in various irAEs similar to autoimmune diseases. Gastrointestinal toxicity, endocrine toxicity, and dermatologic toxicity are common side effects. Neurotoxicity, cardiotoxicity, and pulmonary toxicity are relatively rare but can be fatal. ICI-related gastrointestinal toxicity, dermatologic toxicity, and hypophysitis are more common with anti- CTLA-4 agents. ICI-related pulmonary toxicity, thyroid dysfunction, and myasthenia gravis are more common with PD-1/PD-L1 inhibitors. Treatment with systemic steroids is the principal strategy against irAEs. The use of immune-modulatory agents should be considered in case of no response to the steroid therapy. Treatment under the supervision of multidisciplinary specialists is also essential, because the symptoms and treatments of irAEs could involve many organs. Thus, this review focuses on the mechanism, clinical presentation, incidence, and treatment of various irAEs.

• Journal of Periodontal and Implant Science
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• v.43 no.1
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• pp.3-11
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• 2013

Periodontitis is a chronic inflammation of periodontal tissue caused by subgingival plaque-associated bacteria. Periodontitis has long been understood to be the result of an excessive host response to plaque bacteria. In addition, periodontal pathogens have been regarded as the causative agents that induce a hyperinflammatory response from the host. In this brief review, host-microbe interaction of nonperiodontopathic versus periodontopathic bacteria with innate immune components encountered in the gingival sulcus will be described. In particular, we will describe the susceptibility of these microbes to antimicrobial peptides (AMPs) and phagocytosis by neutrophils, the induction of tissue-destructive mediators from neutrophils, the induction of AMPs and interleukin (IL)-8 from gingival epithelial cells, and the pattern recognition receptors that mediate the regulation of AMPs and IL-8 in gingival epithelial cells. This review indicates that true periodontal pathogens are poor activators/suppressors of a host immune response, and they evade host defense mechanisms.