• Environmental Analysis Health and Toxicology
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• v.3 no.3_4
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• pp.17-28
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• 1988

The effects of perilla oil diet on the immune response in mice have been studied. ICR male mice were divided into 4 groups and were fed on the experimental diet for 4 weeks. Mice were sensitized and challenged with sheep red blood cell (S-RBC). Immune response were evaluated by antibody production, Arthus reaction, delayed type hypersensitivity (DTH), Rosette forming cell (RFC) and macrophage activity. The weight of body, liver, thymus and spleen were measured. The body weight was increased but thymus weight was not altered by them. The perilla oil diet decreased the weight of liver and spleen in mice. It reduced antibody production, Arthus reaction, DTH and RFC, macrophage activity. These results showed that the high perilla oil diet decresed more humoral and celluar immune response than the low perilla oil diet. It decreased the phagocytic activity on the reticuloendothelial system in mice.

• Journal of Korean Academy of Nursing
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• v.21 no.1
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• pp.5-15
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• 1991

The present study was undertaken in an effort to investigate the effects of alcohol on survival of mice and on their humoral and cellular immune responses, The immune responses examined were Arthus and delayed-type hyperrsnesitivity(DTH) reactions to sheep red blood cells(SRBC), contact hypersensitivity to dinitrofluorobenzend(DNFB), antibody response to thymus - dependent SRBC and to thymus -independent polyvinylpyroridone(PVP), and the recovery of Crytococcus neoformans from the liver, spleen, kidney and brain of experimentally infected mice. The administration of ethanol concentrations of 20% or less did not cause any change in survival rates as compared withs saline injected control group. In general, ethanol administration inhibited the Arthus and DTH reactions to SRBC, contact hypersensitivity to DNFB, and antibody response to both SRBC and PVP and it also decreased the resistance of mice to C. neoformans infection. Taken together, the present study stongly suggested that ethanol inhibits immune response and decrease the resistance of mice to C. neoformans infection.

• YAKHAK HOEJI
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• v.45 no.6
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• pp.670-676
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• 2001

Effect of the butanol fraction of Astragali Radix (BFAR) on the humoral immune response were investigated in ICR mice. Mice were divided into 4 groups and BFAR at doses of 5,25 and 125 mg/kg were administered orally to mice daily for 3 weeks, and the normal animals were given vehicle. The results of this study are summarized as follows; the relative weight of spleen was markedly increased by BFAR treatment, compared with that in normal mice. However, the body weight gain and the relative weight of liver were not affected. Splenic plaque forming cells and hemagglutination titers to sheep red blood cells, and the secondary IgG antibody response to bovine serum albumin were also dose-dependently enhanced by BFAR treatment. In these mice, BFAR did not increase serum alanine aminotransferase total protein, sect albumin and albumin/globulin ratio when compared with those in normal mice. Thus, these findings indicate that BFAR significantly enhances humoral immune response to antigen in concentrations that do not affected liver function.

• International Journal of Industrial Entomology and Biomaterials
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• v.45 no.2
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• pp.43-48
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• 2022

Bombyx mori is a representative industrial insect and is used in silk production. Additionally, it serves as an insect model in molecular studies. To date, various molecular studies on its physiological characteristics, including the innate immune response and cuticular melanization, have been conducted. The melanization, including cuticular melanization, in insects is controlled by the prophenoloxidase-activating system, which is also involved in their innate immune response. In this review, to better understand the molecular mechanisms underlying the prophenoloxidase-activating system in the silkworm, the roles of five biomolecules, namely tyrosine hydroxylase, prophenoloxidase-activating enzyme, phenoloxidase, serine protease homolog, and immulectin, are discussed.

• Journal of Acupuncture Research
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• v.17 no.1
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• pp.169-174
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• 2000

The immune response of Bee Venom Therapy is commonly appear in clinics. It is whole body delayed allergy type and generally like fatigue. Therefore, in order to analysis the clinical form, we have observed immune response of 100 patients who visited Sangji University Oriental Medical Hospital and treated Bee Venom Therapy over 10 times from November 1998 to October 1999. The results were summarized as follows. 1. The distribution of Sex was 60 females, 40 males, and the average of patients age was $50.6{\pm}1.5years$. 2. The distribution of disease was degenerative arthritis, HIVD of L-spine, RA, etc. 3. The total treated time is 2765 and is observed 361 immume responses. 4. The average of keeping time in immume response is $11.8{\pm}0.6(hr)$, and the cases of over 24hrs is occupied 24.0%. 5. In the correlation between treated times and immume response is generally in inverse proportion. 6. The general aspect of immume response is chilling, heating, powerless, headache, dizziness, etc. 7. $M{\ddot{u}}ller$ Grade II-III was observed only 1%.

• Parasites, Hosts and Diseases
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• v.55 no.6
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• pp.587-599
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• 2017

The immune response against Trichinella spiralis at the intestinal level depends on the $CD4^+$ T cells, which can both suppress or promote the inflammatory response through the synthesis of diverse cytokines. During the intestinal phase, the immune response is mixed (Th1/Th2) with the initial predominance of the Th1 response and the subsequent domination of Th2 response, which favor the development of intestinal pathology. In this context, the glucocorticoids (GC) are the pharmacotherapy for the intestinal inflammatory response in trichinellosis. However, its therapeutic use is limited, since studies have shown that treatment with GC suppresses the host immune system, favoring T. spiralis infection. In the search for novel pharmacological strategies that inhibit the Th1 immune response (proinflammatory) and assist the host against T. spiralis infection, recent studies showed that resiniferatoxin (RTX) had anti-inflammatory activity, which decreased the serum levels of IL-12, $INF-{\gamma}$, $IL-1{\beta}$, $TNF-{\alpha}$, NO, and $PGE_2$, as well the number of eosinophils in the blood, associated with decreased intestinal pathology and muscle parasite burden. These researches demonstrate that RTX is capable to inhibit the production of Th1 cytokines, contributing to the defense against T. spiralis infection, which places it as a new potential drug modulator of the immune response.

• Experimental and Molecular Medicine
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• v.50 no.12
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• pp.10.1-10.11
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• 2018

Cancer growth and progression are associated with immune suppression. Cancer cells have the ability to activate different immune checkpoint pathways that harbor immunosuppressive functions. Monoclonal antibodies that target immune checkpoints provided an immense breakthrough in cancer therapeutics. Among the immune checkpoint inhibitors, PD-1/PD-L1 and CTLA-4 inhibitors showed promising therapeutic outcomes, and some have been approved for certain cancer treatments, while others are under clinical trials. Recent reports have shown that patients with various malignancies benefit from immune checkpoint inhibitor treatment. However, mainstream initiation of immune checkpoint therapy to treat cancers is obstructed by the low response rate and immune-related adverse events in some cancer patients. This has given rise to the need for developing sets of biomarkers that predict the response to immune checkpoint blockade and immune-related adverse events. In this review, we discuss different predictive biomarkers for anti-PD-1/PD-L1 and anti-CTLA-4 inhibitors, including immune cells, PD-L1 overexpression, neoantigens, and genetic and epigenetic signatures. Potential approaches for further developing highly reliable predictive biomarkers should facilitate patient selection for and decision-making related to immune checkpoint inhibitor-based therapies.

• IMMUNE NETWORK
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• v.11 no.1
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• pp.11-41
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• 2011

The discovery of microRNA (miRNA) is one of the major scientific breakthroughs in recent years and has revolutionized current cell biology and medical science. miRNAs are small (19~25nt) noncoding RNA molecules that post-transcriptionally regulate gene expression by targeting the 3' untranslated region (3'UTR) of specific messenger RNAs (mRNAs) for degradation of translation repression. Genetic ablation of the miRNA machinery, as well as loss or degradation of certain individual miRNAs, severely compromises immune development and response, and can lead to immune disorders. Several sophisticated regulatory mechanisms are used to maintain immune homeostasis. Regulatory T (Treg) cells are essential for maintaining peripheral tolerance, preventing autoimmune diseases and limiting chronic inflammatory diseases. Recent publications have provided compelling evidence that miRNAs are highly expressed in Treg cells, that the expression of Foxp3 is controlled by miRNAs and that a range of miRNAs are involved in the regulation of immunity. A large number of studies have reported links between alterations of miRNA homeostasis and pathological conditions such as cancer, cardiovascular disease and diabetes, as well as psychiatric and neurological diseases. Although it is still unclear how miRNA controls Treg cell development and function, recent studies certainly indicate that this topic will be the subject of further research. The specific circulating miRNA species may also be useful for the diagnosis, classification, prognosis of diseases and prediction of the therapeutic response. An explosive literature has focussed on the role of miRNA. In this review, I briefly summarize the current studies about the role of miRNAs in Treg cells and in the regulation of the innate and adaptive immune response. I also review the explosive current studies about clinical application of miRNA.

• 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.15 no.1
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• pp.1-8
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• 2015

Innate immune cells survey antigenic materials beneath our body surfaces and provide a front-line response to internal and external danger signals. Dendritic cells (DCs), a subset of innate immune cells, are critical sentinels that perform multiple roles in immune responses, from acting as principal modulators to priming an adaptive immune response through antigen-specific signaling. In the gut, DCs meet exogenous, non-harmful food antigens as well as vast commensal microbes under steady-state conditions. In other instances, they must combat pathogenic microbes to prevent infections. In this review, we focus on the function of intestinal DCs in maintaining intestinal immune homeostasis. Specifically, we describe how intestinal DCs affect IgA production from B cells and influence the generation of unique subsets of T cell.