• Journal of the Korean society of biological therapies in psychiatry
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• v.24 no.3
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• pp.142-155
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• 2018

Insomnia in patients with hematopoietic stem cell transplantation(HSCT) has been underdiagnosed and undertreated. This study reviewed the frequency, characteristics, physical and psychological effects, and treatments of insomnia in HSCT patients to highlight clinical importance in this specialized population. Furthermore, the authors intended to suggest a model that would conceptualize insomnia in the context of HSCT. In the pre-transplant period, about half of patients with HSCT suffered from sleep disturbance. A substantial number of patients experienced distressing insomnia during the HSCT procedure and recovered to the level of the pre-transplant period. However, sleep disruption could be a chronic symptom in HSCT survivors and could negatively impact quality of control, cancer-related fatigue(CRF), immune function, and psychological distress. The 3P's model(Predisposing, Precipitating, Perpetuating) explains insomnia in cancer population and could be also relevant to HSCT patients with specific consideration of CRF, graft-versus-host diseases, specific properties of hematological disease, and protective isolated milieu. Effective treatment of insomnia in HSCT includes non-pharmacological(e.g., cognitive behavioral therapy, environmental modification) and pharmacological interventions. The decision of pharmacological treatment should be based on the issue of safety due to high risk of potential drug-drug interactions. Screening, treatment, and further research of insomnia in HSCT patients using validated subjective and/or objective measures are warranted.

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.5
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• pp.1020-1024
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• 2002

The purpose of this research was to investigate the effects of Kamidaebo-tang water extract (KDT) on murine peritoneal macrophages. KDT (50 or 250 mg/kg) was administerd p.o. once a day for 7 days to mice. KDT increased the production of tumor necrosis factor-α and nitric oxide from murine peritoneal macrophages, but decreased the production of interleukin-1β. Also, KDT enhanced the production of lucigenin chemiluminescence from peritoneal macrophages. These results suggest that KDT enhances the non-specific immune response via increase of tumor necrosis factor-α and nitric oxide and phagocytic activity from peritoneal macrophages.

• Mycobiology
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• v.48 no.1
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• pp.1-8
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• 2020

Pentraxin 3 (PTX3) is a soluble pattern recognition receptor (PRR), which is produced by several kinds of cells, such as neutrophils, dendritic cells, macrophages, and epithelial cells. PTX3 is known to play an important protective effect against Aspergillus. Genetic linkage in gene-targeted mice and human PTX3 plays a non-redundant role in the immune protection against specific pathogens, especially Aspergillus. Recent studies have shown that the polymorphism of PTX3 is associated with increased susceptibility to invasive aspergillosis (IA). In this review, we provide an overview of these studies that underline the potential of PTX3 in diagnosis and therapy of IA.

• Molecules and Cells
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• v.44 no.5
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• pp.301-309
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• 2021

Innate lymphoid cells (ILCs) are the most recently discovered family of innate immune cells. ILCs can be categorized into three groups on the basis of the transcription factors that direct their functions and the cytokines they produce. Notably, these functions parallel the effector functions of T lymphocytes. ILCs play a frontline role in host defense and tissue homeostasis by responding rapidly to environmental factors, conducting effector responses in a tissue-specific manner, and interacting with hematopoietic and non-hematopoietic cells throughout the body. Moreover, recent studies reveal that ILCs are involved in development of various inflammatory diseases, such as respiratory diseases, autoimmune diseases, or cancer. In this review, we discuss the recent findings regarding the biology of ILCs in health and inflammatory diseases.

• IMMUNE NETWORK
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• v.22 no.6
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• pp.45.1-45.15
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• 2022

Asthma is a chronic airway inflammatory disease characterized by reversible airway obstruction and airway hyperreactivity to various environmental stimuli, leading to recurrent cough, dyspnea, and wheezing episodes. Regarding inflammatory mechanisms, type 2/eosinophilic inflammation along with activated mast cells is the major one; however, diverse mechanisms, including structural cells-derived and non-type 2/neutrophilic inflammations are involved, presenting heterogenous phenotypes. Although most asthmatic patients could be properly controlled by the guided treatment, patients with severe asthma (SA; classified as a treatment-refractory group) suffer from uncontrolled symptoms with frequent asthma exacerbations even on regular anti-inflammatory medications, raising needs for additional controllers, including biologics that target specific molecules found in asthmatic airway, and achieving the precision medicine for asthma. This review summarizes the immunologic basis of airway inflammatory mechanisms and current biologics for SA in order to address unmet needs for future targets.

• IMMUNE NETWORK
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• v.21 no.4
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• pp.28.1-28.14
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• 2021

Lung-resident memory T cells (T_RM) play an essential role in protecting against pulmonary virus infection. Parenteral administration of DNA vaccine is generally not sufficient to induce lung CD8 T_RM cells. This study investigates whether intramuscularly administered DNA vaccine expressing the nucleoprotein (NP) induces lung T_RM cells and protects against the influenza B virus. The results show that DNA vaccination poorly generates lung T_RM cells and massive secondary effector CD8 T cells entering the lungs after challenge infection do not offer sufficient protection. Nonetheless, intranasal administration of non-replicating adenovirus vector expressing no Ag following priming DNA vaccination deploys NP-specific CD8 T_RM cells in the lungs, which subsequently offers complete protection. This novel 'prime and deploy' strategy could be a promising regimen for a universal influenza vaccine targeting the conserved NP Ag.

• Biomolecules & Therapeutics
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• v.32 no.4
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• pp.424-431
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• 2024

Among the therapeutic strategies in cancer immunotherapy-such as immune-modulating antibodies, cancer vaccines, or adoptive T cell transfer-T cells have been an attractive target due to their cytotoxicity toward tumor cells and the tumor antigen-specific binding of their receptors. Leveraging the unique properties of T cells, chimeric antigen receptor-T cells and T cell receptor (TCR)-T cells were developed through genetic modification of their receptors, enhancing the specificity and effectiveness of T cell therapy. Adoptive cell transfer of chimeric antigen receptor-T cells has been successful for the treatment of hematological malignancies. To expand T cell therapy to solid tumors, T cells are modified to express defined TCR targeting tumor associated antigen, which is called TCR-T therapy. This review discusses anti-tumor T cell therapies, with a focus on engineered TCR-T cell therapy. We outline the characteristics of TCR-T cell therapy and its clinical application to non-hematological malignancies.

• Animal cells and systems
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• v.3 no.3
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• pp.337-341
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• 1999

Hepatitis C virus (HCV) is a positive strand RNA virus of the Flaviviridae family and the major cause of post-transfusion non-A, non-B hepatitis. Vaccine development for HCV is essential but has been slowed by poor understanding of the type of immunity that naturally terminates HCV infection. The DNA-based immunization technique offers the potential advantage of including cellular immune responses against conserved internal proteins of a virus, as well as the generation of antibodies to viral surface proteins. Here, we demonstrate that cell lines expressing the HCV core and/or NS3 proteins can induce a specific CTL response in mice, and these results suggest a possibility that the HCV core and NS3 DNA can be used to induce CTL activity against the antigen in mice and can be further developed as a therapeutic and preventive DNA vaccine.

• Journal of Chest Surgery
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• v.12 no.1
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• pp.16-22
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• 1979

Clinical evaluation of contact sensitization to 2, 4-dinitro-chlorobenzene [DNCB] was performed in 2 groups: group A [30 patients with non-malignant disease] and group B [30 patients with bronchogenic carcinoma]. Initial sensitization was elicited out by applying 2, 000 ug of DNCB to skin surface of the both group A and B. Subsequently a relatively weak challenge dose, 200 ug of DNCB, was applied 14 days later, showing the satisfactory results of sensitization with minimizing non-specific irritative inflammatory skin response. Delayed cutaneous hypersensitivity reactions shown by spontaneous flare phenomena appeared at the challenge site, and they were assessed 48 hours later. The reaction were graded from +1 to +4 according to the degree of flare or vesicular reaction. The results were as follows: 1. 28 cases [93%] of group A, however, only 18 cases [67%] of group B exhibited delayed cutaneous hypersensitivity reaction to DNCB contact sensitization [P<0.02]. 2. Of group A, the delayed cutaneous hypersensitivity reactions above +2 of DNCB score were 25 cases [83%], meanwhile 11 cases [37%] in group B [P<0.001]. 3. Undifferentiated carcinomas showed highest incidence of anergy to DNCB contact sensitization in the all histologic types of group B. 4. In group B, 8 [42%] of 19 cases who react to DNCB were resectable, whereas only 2 [18 %] of 11 cases who failed to react to DNCB were resectable for curative cancer surgery. These study suggests that cellular immune reaction of group B was depressed remarkably comparing with that of group A.

• Molecules and Cells
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• v.37 no.4
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• pp.286-294
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• 2014

Mammalian polo-like kinase 1 (Plk1) has been studied intensively as a key regulator of various cell cycle events that are critical for proper M-phase progression. The polobox domain (PBD) present in Plk1's C-terminal noncatalytic region has been shown to play a central role in targeting the N-terminal kinase domain of Plk1 to specific subcellular locations. Subsequent studies reveal that PBD binds to a phosphorylated motif generated by one of the two mechanisms - self-priming by Plk1 itself or non-self-priming by a Pro-directed kinase, such as Cdc2. Here, we comparatively review the differences in the biochemical steps of these mechanisms and discuss their physiological significance. Considering the diverse functions of Plk1 during the cell cycle, a better understanding of how the catalytic activity of Plk1 functions in concert with its cisacting PBD and how this coordinated process is intricately regulated to promote Plk1 functions will be important for providing new insights into different mechanisms underlying various Plk1-mediated biological events that occur at the multiple stages of the cell cycle.