• The Korean Journal of Physiology and Pharmacology
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• v.19 no.6
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• pp.479-484
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• 2015

NOD2 (nucleotide-binding and oligomerization domain 2) was initially reported as a susceptibility gene for Crohn's disease, with several studies focused on elucidating its molecular mechanism in the progression of Crohn's disease. We now know that NOD2 is an intracellular bacterial sensing receptor, and that MDP-mediated NOD2 activation drives inflammatory signaling. Various mutations in NOD2 have been reported, with NOD2 loss of function being associated with the development of Crohn's disease and other autoimmune diseases. These results suggest that NOD2 not only has an immune stimulatory function, but also an immune regulatory function. Atherosclerosis is a chronic inflammatory disease of the arterial wall; its pathologic progression is highly dependent on the immune balance. This immune balance is regulated by infiltrating monocytes and macrophages, both of which express NOD2. These findings indicate a potential role of NOD2 in atherosclerosis. The purpose of this review is to outline the known roles of NOD2 signaling in the pathogenesis of atherosclerosis.

• Clinical and Experimental Pediatrics
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• v.58 no.7
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• pp.239-244
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• 2015

The complement system is part of the innate immune response and as such defends against invading pathogens, removes immune complexes and damaged self-cells, aids organ regeneration, confers neuroprotection, and engages with the adaptive immune response via T and B cells. Complement activation can either benefit or harm the host organism; thus, the complement system must maintain a balance between activation on foreign or modified self surfaces and inhibition on intact host cells. Complement regulators are essential for maintaining this balance and are classified as soluble regulators, such as factor H, and membrane-bound regulators. Defective complement regulators can damage the host cell and result in the accumulation of immunological debris. Moreover, defective regulators are associated with several autoimmune diseases such as atypical hemolytic uremic syndrome, dense deposit disease, age-related macular degeneration, and systemic lupus erythematosus. Therefore, understanding the molecular mechanisms by which the complement system is regulated is important for the development of novel therapies for complement-associated diseases.

• Korean Journal of Biological Psychiatry
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• v.15 no.3
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• pp.147-151
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• 2008

This review briefly summarizes the relevant knowledge of psychoneuroimmunological basis for neuroimmunology, with particular emphasis on bidirectional neural-immune interactions. The immune system and the nervous system maintain extensive communication, including hardwiring of sympathetic and parasympathetic nerves to lymphoid organs. Immune system is modulated by various neurotransmitters such as acetylcholine, norepinephrine, substance P and histamine. Neuroendocrine hormones such as corticotrophin-releasing hormone(CRH) or substance P regulate cytokine balance. The immune system modulates brain activity including sleep and body temperature. Recent studies have revealed that psychological factors which influence immunity and immune-related disease may modulate brain-to -immune interaction. But, we still await the scientific research and evidences to prove whether or how behavioral or treatment intervention of stress can influence the development, progress or prevention of a specific disease.

• Molecules and Cells
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• v.44 no.6
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• pp.408-421
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• 2021

The outbreak of coronavirus disease 2019 (COVID-19) has not only affected human health but also diverted the focus of research and derailed the world economy over the past year. Recently, vaccination against COVID-19 has begun, but further studies on effective therapeutic agents are still needed. The severity of COVID-19 is attributable to several factors such as the dysfunctional host immune response manifested by uncontrolled viral replication, type I interferon suppression, and release of impaired cytokines by the infected resident and recruited cells. Due to the evolving pathophysiology and direct involvement of the host immune system in COVID-19, the use of immune-modulating drugs is still challenging. For the use of immune-modulating drugs in severe COVID-19, it is important to balance the fight between the aggravated immune system and suppression of immune defense against the virus that causes secondary infection. In addition, the interplaying events that occur during virus-host interactions, such as activation of the host immune system, immune evasion mechanism of the virus, and manifestation of different stages of COVID-19, are disjunctive and require thorough streamlining. This review provides an update on the immunotherapeutic interventions implemented to combat COVID-19 along with the understanding of molecular aspects of the immune evasion of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which may provide opportunities to develop more effective and promising therapeutics.

• Journal of Microbiology and Biotechnology
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• v.29 no.11
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• pp.1739-1744
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• 2019

The present study evaluates the immunomodulatory effect of Bifidobacterium longum KACC 91563 in murine primary splenocytes and macrophages. B. longum KACC 91563 regulated T- and B-cell proliferation and inhibited the Th1 (IL-2, IFN-γ)/Th2 (IL-4, IL-10) cytokine imbalance and immune cytokine production. Moreover, immunoglobulin E (IgE) levels were significantly lower after treatment with B. longum KACC 91563. These findings suggest that B. longum KACC 91563 could modulate the systemic immune system toward both IgE production and regulation of the Th1/Th2 balance.

• Journal of Electrical Engineering and Technology
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• v.8 no.5
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• pp.959-968
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• 2013

This paper presents a new approach with artificial immune system algorithm to solve the profit based unit commitment problem. The objective of this work is to find the optimal generation scheduling and to maximize the profit of generation companies (Gencos) when subjected to various constraints such as power balance, spinning reserve, minimum up/down time and ramp rate limits. The proposed hybrid method is developed through adaptive search which is inspired from artificial immune system and genetic algorithm to carry out profit maximization of generation companies. The effectiveness of the proposed approach has been tested for different Gencos consists of 3, 10 and 36 generating units and the results are compared with the existing methods.

• Toxicological Research
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• v.25 no.4
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• pp.159-173
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• 2009

Nuclear factor erythroid derived 2-related factor-2 (Nrf2) is a master transcription regulator of antioxidant and cytoprotective proteins that mediate cellular defense against oxidative and inflammatory stresses. Disruption of cellular stress response by Nrf2 deficiency causes enhanced susceptibility to infection and related inflammatory diseases as a consequence of exacerbated immune-mediated hypersensitivity and autoimmunity. The cellular defense capacity potentiated by Nrf2 activation appears to balance the population of $CD4^+$ and $CD8^+$ of lymph node cells for proper innate immune responses. Nrf2 can negatively regulate the activation of pro-inflammatory signaling molecules such as p38 MAPK, NF-${\kappa}B$, and AP-1. Nrf2 subsequently functions to inhibit the production of pro-inflammatory mediators including cytokines, chemokines, cell adhesion molecules, matrix metalloproteinases, COX-2 and iNOS. Although not clearly elucidated, the antioxidative function of genes targeted by Nrf2 may cooperatively regulate the innate immune response and also repress the expression of pro-inflammatory mediators.

• BMB Reports
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• v.52 no.4
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• pp.259-264
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• 2019

Social requirements are needed for living in an aging society and individual longevity. Among them, improved health and medical cares, appropriate for an aging society are strongly demanded. Human cord blood-derived plasma (hUCP) has recently emerged for its unique anti-aging effects. In this study, we investigated brain rejuvenation, particularly olfactory function, that could be achieved by a systemic administration of young blood and its underlying mechanisms. Older than 24-month-old mice were used as an aged group and administered with intravenous injection of hUCP repetitively, eight times. Anti-aging effect of hUCP on olfactory function was evaluated by buried food finding test. To investigate the mode of action of hUCP, brain, serum and spleen of mice were collected for further ex vivo analyses. Systemic injection of hUCP improved aging-associated olfactory deficits, reducing time for finding food. In the brain, although an infiltration of activated microglia and its expression of cathepsin S remarkably decreased, significant changes of proinflammatory factors were not detected. Conversely, peripheral immune balance distinctly switched from predominance of Type 1 helper T (Th1) cells to alternative regulatory T cells (Tregs). These findings indicate that systemic administration of hUCP attenuates age-related neuroinflammation and subsequent olfactory dysfunction by modulating peripheral immune balance toward Treg cells, suggesting another therapeutic function and mechanism of hUCP administration.

• IMMUNE NETWORK
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• v.14 no.4
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• pp.187-200
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• 2014

Herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) are the most common cause of genital ulceration in humans worldwide. Typically, HSV-1 and 2 infections via mucosal route result in a lifelong latent infection after peripheral replication in mucosal tissues, thereby providing potential transmission to neighbor hosts in response to reactivation. To break the transmission cycle, immunoprophylactics and therapeutic strategies must be focused on prevention of infection or reduction of infectivity at mucosal sites. Currently, our understanding of the immune responses against mucosal infection of HSV remains intricate and involves a balance between innate signaling pathways and the adaptive immune responses. Numerous studies have demonstrated that HSV mucosal infection induces type I interferons (IFN) via recognition of Toll-like receptors (TLRs) and activates multiple immune cell populations, including NK cells, conventional dendritic cells (DCs), and plasmacytoid DCs. This innate immune response is required not only for the early control of viral replication at mucosal sites, but also for establishing adaptive immune responses against HSV antigens. Although the contribution of humoral immune response is controversial, $CD4^+$ Th1 T cells producing IFN-${\gamma}$ are believed to play an important role in eradicating virus from the hosts. In addition, the recent experimental successes of immunoprophylactic and therapeutic compounds that enhance resistance and/or reduce viral burden at mucosal sites have accumulated. This review focuses on attempts to modulate innate and adaptive immunity against HSV mucosal infection for the development of prophylactic and therapeutic strategies. Notably, cells involved in innate immune regulations appear to shape adaptive immune responses. Thus, we summarized the current evidence of various immune mediators in response to mucosal HSV infection, focusing on the importance of innate immune responses.

• KSII Transactions on Internet and Information Systems (TIIS)
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• v.4 no.6
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• pp.1273-1293
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• 2010

Immune-inspired intrusion detection is a promising technology for network security, and well known for its diversity, adaptation, self-tolerance, etc. However, scalability and coverage are two major drawbacks of the immune-inspired intrusion detection systems (IIDSes). In this paper, we propose an IIDS framework, named GEP-IIDS, with improved basic system elements to address these two problems. First, an additional bio-inspired technique, gene expression programming (GEP), is introduced in detector (corresponding to detection rules) representation. In addition, inspired by the avidity model of immunology, new avidity/affinity functions taking the priority of attributes into account are given. Based on the above two improved elements, we also propose a novel immune algorithm that is capable of integrating two bio-inspired mechanisms (i.e., negative selection and positive selection) by using a balance factor. Finally, a pruning algorithm is given to reduce redundant detectors that consume footprint and detection time but do not contribute to improving performance. Our experimental results show the feasibility and effectiveness of our solution to handle the scalability and coverage problems of IIDS.