• 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.

• IMMUNE NETWORK
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• v.24 no.4
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• pp.30.1-30.16
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• 2024

Pregnancy represents an immunological paradox where the maternal immune system must tolerate the semi-allogeneic fetus expressing paternally-derived Ags. Accumulating evidence over decades has revealed that successful pregnancy requires the active development of robust immune tolerance mechanisms. This review outlines the multi-layered processes that establish fetomaternal tolerance, including the physical barrier of the placenta, restricted chemokine-mediated leukocyte trafficking, lack of sufficient alloantigen presentation, the presence of immunosuppressive regulatory T cells and tolerogenic decidual natural killer cells, expression of immune checkpoint molecules, specific glycosylation patterns conferring immune evasion, and unique metabolic/hormonal modulations. Interestingly, many of the strategies that enable fetal tolerance parallel those employed by cancer cells to promote angiogenesis, invasion, and immune escape. As such, further elucidating the mechanistic underpinnings of fetal-maternal tolerance may reciprocally provide insights into developing novel cancer immunotherapies as well as understanding the pathogenesis of gestational complications linked to dysregulated tolerance processes.

• Animal Bioscience
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• v.34 no.3_spc
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• pp.321-337
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• 2021

The global population has increased with swift urbanization in developing countries, and it is likely to result in a high demand for animal-derived protein-rich foods. Animal farming has been constantly affected by various stressful conditions, which can be categorized into physical, environmental, nutritional, and biological factors. Such conditions could be exacerbated by banning on the use of antibiotics as a growth promoter together with a pandemic situation including, but not limited to, African swine fever, avian influenza, and foot-and-mouth disease. To alleviate these pervasive tension, various immunomodulants have been suggested as alternatives for antibiotics. Various studies have investigated how stressors (i.e., imbalanced nutrition, dysbiosis, and disease) could negatively affect nutritional physiology in chickens. Importantly, the immune system is critical for host protective activity against pathogens, but at the same time excessive immune responses negatively affect its productivity. Yet, comprehensive review articles addressing the impact of such stress factors on the immune system of chickens are scarce. In this review, we categorize these stressors and their effects on the immune system of chickens and attempt to provide immunomodulants which can be a solution to the aforementioned problems facing the chicken industry.

• The Journal of Internal Korean Medicine
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• v.43 no.3
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• pp.327-343
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• 2022

Objective: The purpose of this study was to develop a standard tool for identifying idiopathic pulmonary fibrosis patterns. Methods: Textbooks, published literature, and references with comments on patterns were reviewed. Using the Delphi method, we determined pattern identification based on the advice of a committee consisting of 11 Korean respiratory internal medicine professors. Results: Four pattern identifications were selected by the Delphi method: qi difficiency (氣虛), yin difficiency (陰虛), phlegm dampness (痰飮), blood stasis (瘀血). The tool was developed in a question-and-answer format containing 38 questions. Conclusions: An IPF pattern identification tool that can analyze IPF patterns for standardized diagnostics was developed with the consent of experts. Further research is needed on its reliability.

• Proceedings of the Plant Resources Society of Korea Conference
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• 2023.04a
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• pp.45-45
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• 2023

Autophagy contributes to enhancing the immune system (innate and adaptive immune system) against foreign pathogens. Autophagy of macrophages is used as a major indicator for developing vaccine adjuvants to increase the adaptive immune response. In this study, RAL increased the production of immunostimulatory mediators and phagocytotic activity in RAW264.7 cells. RAL increased p62/SQSTM1 expression. Inhibition of TLR4, JNK, and PI3K/AKT blocked RAL-mediated increase of p62/SQSTM1. RAL activated JNK and PI3K/AKT signaling. RAL-mediated activation of JNK and PI3K/AKT signaling was reversed by TLR4 inhibition. Taken together, it is believed that RAL-mediated autophagy may be dependent on activating via TLR4-dependent activation of JNK and PI3K/AKT signaling in macrophages.

• Clinical and Experimental Pediatrics
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• v.50 no.12
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• pp.1165-1172
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• 2007

Self/non-self discrimination and unresponsiveness to self is the fundamental properties of the immune system. Self-tolerance is a state in which the individual is incapable of developing an immune response to an individual's own antigens and it underlies the ability to remain tolerant of individual's own tissue components. Several mechanisms have been postulated to explain the tolerant state. They can be broadly classified into two groups: central tolerance and peripheral tolerance. Several mechanisms exist, some of which are shared between T cells and B cells. In central tolerance, the recognition of self-antigen by lymphocytes in bone marrow or thymus during development is required, resulting in receptor editing (revision), clonal deletion, anergy or generation of regulatory T cells. Not all self-reactive B or T cells are centrally purged from the repertoire. Additional mechanisms of peripheral tolerance are required, such as anergy, suppression, deletion or clonal ignorance. Tolerance is antigen specific. Generating and maintaining the self-tolerance for T cells and B cells are complex. Failure of self-tolerance results in immune responses against self-antigens. Such reactions are called autoimmunity and may give rise to autoimmune diseases. Development of autoimmune disease is affected by properties of the genes of the individual and the environment, both infectious and non-infectious. The host's genes affect its susceptibility to autoimmunity and the environmental factors promote the activation of self-reactive lymphocytes, developing the autoimmunity. The changes in participating antigens (epitope spreading), cells, cytokines or other inflammatory mediators contribute to the progress from initial activation to a chronic state of autoimmune diseases.

• Toxicological Research
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• v.17
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• pp.211-216
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• 2001

Drugs can have various adverse effects on the immune system including unintended immun-osuppression, induction of both drug-specific immune responses (including drug allergies) and non-specific immunostimulation (including autoimmune reactions), and direct activation of effector mechanisms (such as histamine release). As a practical matter, the Center for Drug Evaluation (CDER) relies on standard non-clinical toxicology studies to detect unintended immunosuppression. Specific assays using guinea pigs and mice are available to identify drugs that can induce immune-mediated dermal hypersensitivity reactions. Respiratory and systemic hypersensitivity and autoimmune reactions are more difficult to model in non-clinical studies. Unintended nonspecific immunstimulation can be detected in animal studies. CDER is currently developing specific guidance for evaluating potential drug immunotoxicity.

• Journal of the Korean Institute of Intelligent Systems
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• v.13 no.1
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• pp.119-124
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• 2003

In this paper, we modeled positive selection and negative selection that is developing process of cytotoxic T-cell that plays important role in biological immune system. Also, we developed change detection algorithm, which is very Important part in detecting data change by intrusion and data infection by computer virus. Proposed method is the algorithm that produces MHC receptor lot recognizing self and antigen detector for recognizing non-self. Therefore, proposed method detects self and intruder by two type of detectors like real immune system. We show the effectiveness and characteristics of proposed change detection algorithm by simulation about point and block change of self file.

• Journal of the Korea Society of Computer and Information
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• v.14 no.7
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• pp.17-24
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• 2009

Increasing use of information system has led to larger amount of developing expenses and demands on software. Until recent days, the model using regression analysis based on statistical algorithm has been used. However, Machine learning is more investigated now. This paper estimates the software cost using SVR(Support Vector Regression). a sort of machine learning technique. Also, it finds the best set of parameters applying immune algorithm. In this paper, software cost estimation is performed by SVR based on immune algorithm while changing populations, memory cells, and number of allele. Finally, this paper analyzes and compares the result with existing other machine learning methods.

• IMMUNE NETWORK
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• v.16 no.4
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• pp.211-218
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• 2016

Due to the increasing prevalence and number of life-threatening cases, food allergy has emerged as a major health concern. The classic immune response seen during food allergy is allergen-specific IgE sensitization and hypersensitivity reactions to foods occur in the effector phase with often severe and deleterious outcomes. Recent research has advanced understanding of the immunological mechanisms occurring during the effector phase of allergic reactions to ingested food. Therefore, this review will not only cover the mucosal immune system of the gastrointestinal tract and the immunological mechanisms underlying IgE-mediated food allergy, but will also introduce cells recently identified to have a role in the hypersensitivity reaction to food allergens. These include IL-9 producing mucosal mast cells (MMC9s) and type 2 innate lymphoid cells (ILC2s). The involvement of these cell types in potentiating the type 2 immune response and developing the anaphylactic response to food allergens will be discussed. In addition, it has become apparent that there is a collaboration between these cells that contributes to an individual's susceptibility to IgE-mediated food allergy.