• The Plant Pathology Journal
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• v.39 no.5
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• pp.449-465
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• 2023

Plants are challenged by various pathogens throughout their lives, such as bacteria, viruses, fungi, and insects; consequently, they have evolved several defense mechanisms. In addition, plants have developed localized and systematic immune responses due to biotic and abiotic stress exposure. Animals are known to activate DNA damage responses (DDRs) and DNA damage sensor immune signals in response to stress, and the process is well studied in animal systems. However, the links between stress perception and immune response through DDRs remain largely unknown in plants. To determine whether DDRs induce plant resistance to pathogens, Arabidopsis plants were treated with bleomycin, a DNA damage-inducing agent, and the replication levels of viral pathogens and growth of bacterial pathogens were determined. We observed that DDR-mediated resistance was specifically activated against viral pathogens, including turnip crinkle virus (TCV). DDR increased the expression level of pathogenesis-related (PR) genes and the total salicylic acid (SA) content and promoted mitogen-activated protein kinase signaling cascades, including the WRKY signaling pathway in Arabidopsis. Transcriptome analysis further revealed that defense-and SA-related genes were upregulated by DDR. The atm-2atr-2 double mutants were susceptible to TCV, indicating that the main DDR signaling pathway sensors play an important role in plant immune responses. In conclusion, DDRs activated basal immune responses to viral pathogens.

• IMMUNE NETWORK
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• v.15 no.3
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• pp.121-124
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• 2015

Now, it has been being accepted that reverse signaling through CD137 ligand (CD137L) plays an important role in vivo during hematopoiesis and in immune regulation. However, due to technical difficulty in dissecting both directional signaling events simultaneously in vivo, most biological activities caused by CD137-CD137L interactions are considered as results from signaling events of the CD137 receptor. To make the story more complex, $CD137^{-/-}$ and $CD137L^{-/-}$ mice have increased or decreased immune responses in a context-dependent manner. In this Mini review, I will try to provide a plausible explanation for how CD137L signaling is controlled during immune responses.

• IMMUNE NETWORK
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• v.21 no.1
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• pp.1.1-1.16
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• 2021

The emergence of a new severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has become a significant health concern worldwide. Undoubtedly, a better understanding of the innate and adaptive immune responses against SARS-CoV-2 and its relationship with the coronavirus disease 2019 (COVID-19) pathogenesis will be the sole basis for developing and applying therapeutics. This review will summarize the published results that relate to innate immune responses against infections with human coronaviruses including SARS-CoV-1 and SARS-CoV-2 in both humans and animal models. The topics encompass the innate immune sensing of the virus to the dysregulation of various innate immune cells during infection and disease progression.

• IMMUNE NETWORK
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• v.16 no.1
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• pp.1-12
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• 2016

Th2 cell immunity is required for host defense against helminths, but it is detrimental in allergic diseases in humans. Unlike Th1 cell and Th17 cell subsets, the mechanism by which dendritic cells modulate Th2 cell responses has been obscure, in part because of the inability of dendritic cells to provide IL-4, which is indispensable for Th2 cell lineage commitment. In this regard, immune cells other than dendritic cells, such as basophils and innate lymphoid cells, have been suggested as Th2 cell inducers. More recently, multiple independent researchers have shown that specialized subsets of dendritic cells mediate Th2 cell responses. This review will discuss the current understanding related to the regulation of Th2 cell responses by dendritic cells and other immune cells.

• IMMUNE NETWORK
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• v.13 no.6
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• pp.227-234
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• 2013

The intestinal immune system has an ability to distinguish between the microbiota and pathogenic bacteria, and then activate pro-inflammatory pathways against pathogens for host defense while remaining unresponsive to the microbiota and dietary antigens. In the intestine, abnormal activation of innate immunity causes development of several inflammatory disorders such as inflammatory bowel diseases (IBD). Thus, activity of innate immunity is finely regulated in the intestine. To date, multiple innate immune cells have been shown to maintain gut homeostasis by preventing inadequate adaptive immune responses in the murine intestine. Additionally, several innate immune subsets, which promote Th1 and Th17 responses and are implicated in the pathogenesis of IBD, have recently been identified in the human intestinal mucosa. The demonstration of both murine and human intestinal innate immune subsets contributing to regulation of adaptive immunity emphasizes the conserved innate immune functions across species and might promote development of the intestinal innate immunity-based clinical therapy.

• IMMUNE NETWORK
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• v.4 no.2
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• pp.73-80
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• 2004

Viruses are obligate intracellular parasites which cause infection by invading and replicating within cells. The immune system has mechanisms which can attack the virus in extracellular and intracellular phase of life cycle, and which involve both non-specific and specific effectors. The survival of viruses depends on the survival of their hosts, and therefore the immune system and viruses have evolved together. Immune responses to viral infection may be variable depending on the site of infection, the mechanism of cell-to-cell spread of virus, physiology of the host, host genetic variation, and environmental condition. Viral infection of cells directly stimulates the production of interferons and they induce antiviral state in the surrounding cells. Complement system is also involved in the elimination of viruses and establishes the first line of defence with other non-specific immunity. During the course of viral infection, antibody is most effective at an early stage, especially before the virus enters its target cells. The virus- specific cytotoxic T lymphocytes are the principal effector cells in clearing established viral infections. But many viruses have resistant mechanism to host immune responses in every step of viral infection to cells. Some viruses have immune evasion mechanism and establish latency or persistency indefinitely. Furthermore antibodies to some viruses can enhance the disease by the second infection. Immune responses to viral infection are very different from those to bacterial infection.

• Journal of Korean Biological Nursing Science
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• v.4 no.2
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• pp.79-92
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• 2002

This study was aimed to analyze the variables measuring stress and immune responses, to identify the relationship between stress and immune responses, and to find out the effect of nursing interventions associated with stress and immune responses by reviewing thirty-four published articles since 1970 in Korea. The articles were selected in the field of nursing, stress management, and masters or doctoral dissertations and limited to human subject. Among these, the thirty-one articles were published since 1996 and mainly distributed in nursing (44.1%) and medicine(44.1%). The prevailing research design was nonequivalent control pre-post experimental design(41.1%). The research subjects were 55.9% for patients and 44.1% for healthy general persons including 20.6% of university students. To evaluate stress, both physiologic and psychosocial measures were adapted together in 35.3% of the articles. The most frequent two variables measuring stress and immune response were cortisol level(15.9%) and number or activity of natural killer cell(25.9%). The relation between stress and immune responses was positive in 4 articles, negative in 9 cases, and none in 12 cases. Decreased stress and enhanced immune function have been found when massage, abdominal breathing, exercise, relaxation, and touch were provided as nursing interventions. The articles to investigate the relationship between stress and immune function were limited and the tested variables were diverse. Also there was no consistent evidence to correlate the stress and immune function at present. Further studies are needed to construct a valid research design and to investigate the relationship between stress and immune responses. Nursing interventions to decrease stress should be developed to result in the increased immune function and the effect of these interventions would be verified.

• Journal of Microbiology and Biotechnology
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• v.32 no.9
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• pp.1086-1097
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• 2022

During the last decades, research and therapeutic methods in cancer treatment have been evolving. As the results, nowadays, cancer patients are receiving several types of treatments, ranging from chemotherapy and radiation therapy to surgery and immunotherapy. In fact, most cancer patients take a combination of current anti-cancer therapies to improve the efficacy of treatment. However, current strategies still cause some side effects to patients, such as pain and depression. Therefore, there is the need to discover better ways to eradicate cancer whilst minimizing side effects. Recently, immunotherapy, particularly immune checkpoint blockade, is rising as an effective anti-cancer treatment. Unlike chemotherapy or radiation therapy, immunotherapy has few side effects and a higher tumor cell removal efficacy depend on cellular immunological mechanisms. Moreover, recent studies suggest that tissue immune responses are regulated by their microbiome composition. Each tissue has their specific microenvironment, which makes their microbiome composition different, particularly in the context of different types of cancer, such as breast, colorectal, kidney, lung, and skin. Herein, we review the current understanding of the relationship of immune responses and tissue microbiome in cancer in both animal and human studies. Moreover, we discuss the cancer-microbiome-immune axis in the context of cancer development and treatment. Finally, we speculate on strategies to control tissue microbiome alterations that may synergistically affect the immune system and impact cancer treatment outcomes.

• Toxicological Research
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• v.6 no.1
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• pp.13-19
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• 1990

The effects of panaxytrion as known to be a cytotoxic substance isolated from Panax ginseng on the immune responses were examined. The i.p. administration of panaxytriol to normal mice for 6 consecutive days as doses of 5, 10 and 20 mg/kg suppressed the increase of body weight dose-dependently but did not affect the weight ratio of immunoorgans to body weight, No significant changes were observed in the humoral immune responses as measured by Arthus reaction and plaque forming cells and in the cellular immune response as measured by delayed hypersensitivity as well as phagocytic activity of reticuloendotherial system. These results suggested that panaxytriol, a cytotoxic substance to cancer cells, has no detrimental effects on the immune function in normal mice.

• YAKHAK HOEJI
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• v.35 no.5
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• pp.401-415
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• 1991

Effects of quercetin on the specific and non-specific immune responses were studied in vivo. Quercetin at a dose of 2.5, 5, 10, 20 and 40 mg/kg were orally administered to ICR male mice once daily for 28 consecutive days. Cyclophosphamide was injected intraperitoneally to ICR mice with a single dose of 5 mg/kg 2 days before secondary immunization. Mice were sensitized and challenged with sheep red blood cells (S-RBC). Immune responses were evaluated by humoral and cellular immune reponses and non-specific immune response. The results of this study were summarized as followings; 1. Quercetin significantly decreased the body weight, and introduced the atrophy of liver, spleen and thymus gland dose-dependently, but increased the numbers of white blood cell. 2. Querectin significantly depressed the hemagglutination titer, Arthus reaction and hemolytic plaque forming cell. 3. Quercetin significantly depressed the delayed type hypersensitivity and rosette forming cell. 4. Quercetin at a dose of 2.5, 5 and 40 mg/kg significantly depressed phagocytic activity. 5. Quercetin at a dose of 10 and 20 mg/kg significantly increased natural killer cell activity.