• IMMUNE NETWORK
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• v.14 no.2
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• pp.67-72
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• 2014

The herpes virus entry mediator (HVEM) is a member of the tumor necrosis factor receptor superfamily (TNFRSF), and therefore it is also known as TNFRSF14 or CD270 (1,2). In recent years, we have focused on understanding HVEM function in the mucosa of the intestine, particularly on the role of HVEM in colitis pathogenesis, host defense and regulation of the microbiota (2-4). HVEM is an unusual TNF receptor because of its high expression levels in the gut epithelium, its capacity to bind ligands that are not members of the TNF super family, including immunoglobulin (Ig) superfamily members BTLA and CD160, and its bi-directional functionality, acting as a signaling receptor or as a ligand for the receptor BTLA. Clinically, Hvem recently was reported as an inflammatory bowel disease (IBD) risk gene as a result of genome wide association studies (5,6). This suggests HVEM could have a regulatory role influencing the regulation of epithelial barrier, host defense and the microbiota. Consistent with this, using mouse models, we have revealed how HVEM is involved in colitis pathogenesis, mucosal host defense and epithelial immunity (3,7). Although further studies are needed, our results provide the fundamental basis for understanding why Hvem is an IBD risk gene, and they confirm that HVEM is a mucosal gatekeeper with multiple regulatory functions in the mucosa.

• Asian-Australasian Journal of Animal Sciences
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• v.19 no.2
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• pp.297-304
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• 2006

Insulin-like growth factor-I (IGF-I) rich fraction, collected components between 1 kDa and 30 kDa, was fractionated from bovine colostral whey using an ultrafiltration membrane. IGF-I was confirmed in the collected IGF-I rich fraction by both SDS-PAGE and Western blotting. The concentration of IGF-I in the IGF-I rich fraction was 10 ng/mg protein. One hundred microliters of the reconstituted IGF-I rich fraction was intraperitoneally injected into ICR male mice for 2 weeks at 24 h intervals. The functions of peritoneal macrophages, including phagocytosis, interleukin (IL)-6 and tumor necrosis factor (TNF)-${\alpha}$ production, and nitric oxide and hydrogen peroxide production, were enhanced significantly by the administration of the IGF-I rich fraction in a dose-dependent manner (p<0.01). The proliferation of Concanavalin (Con) A-stimulated and Lipopolysaccharide (LPS)-stimulated splenocytes was also determined to have been enhanced significantly by the administration of the IGF-I rich fraction in a dose-dependent manner (p<0.01). Our results indicate that the administration of IGF-I rich fraction obtained from bovine colostral whey enhances both innate and acquired immunity for ICR male mice.

• KSBB Journal
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• v.25 no.1
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• pp.97-102
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• 2010

The enhancement of immunity for atopic dermatitis with application of eicosapentaenoic acid (EPA)-loaded liposome was evaluated on NC/Nga mice. The EPA-loaded liposome was coated with thiol-chitosan. The liposomes were characterized with transmission electron microscopy (TEM), surface zeta potential & particle size analyzer (Zeta-PSA) and differential scanning calorimetry (DSC). The loading efficiency of EPA in the liposome was about 4.7%. The particle size of the EPA-Ioaded liposome was about 230 nm. The values of Immunoglobulin E (IgE), interleukin-4 (IL-4), and tumor necrosis factor-$\alpha$ (TNF-$\alpha$) were reduced significantly with application of the EPA-loaded liposome. The interferon-$\gamma$ (IFN-$\gamma$) value was increased with the application effect. It is concluded that EPA loaded liposome have immunity advancing effects in mouse model of atopic dermatitis.

• IMMUNE NETWORK
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• v.4 no.4
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• pp.250-254
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• 2004

Background: It is necessary for human beings to uptake vitamin C through diet or supplements. It is also well-known that vitamin C plays an important role in the prevention of scurvy, enhancement of collagen synthesis and anti-tumor immune response. In addition, there are several recent reports regarding the effective role of vitamin C on the regulation of allergic responses, such as atopic dermatitis and asthma. However, the effective therapeutic and preventive measures using vitamin C are not established yet, since vitamin C is seriously unstable in aqueous solution. Therefore, we have investigated the best way to maintain the stability of vitamin C. Methods: After we making a mixture of polyphenol (0.001, 0.01, 0.1%) and vitamin C (1 mM), the mixtures were placed at room temperature both with/without light protection. And then the concentration of ascorbic acid was measured with HPLC. To analyze the in vivo effect of vitamin C on the regulation of skin allergic reaction, polyphenol (0.1%)-vitamin C (1 mM) mixture was applied to the skin and the production of histamine from mast cell was analyzed by Evans blue dye staining. Results: We have found that the polyphenol has preventive power of oxidation of vitamin C. In addition, the production of histamine was suppressed by the polyphenol (0.1%)-vitamin C (1 mM) mixture. Conclusion: We have reached the conclusion that our study suggests the research guideline for the therapy of atopic dermatitis through vitamin C.

• The Journal of Korean Medicine
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• v.27 no.4
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• pp.30-47
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• 2006

Objective : The present study is aimed to elucidate the effects of Cirsium japonicum var. ussuriense on immunomodulation and the potential as an herbal remedy for cancer treatment. Method : It was performed through measurement of effects Cirsium japonicum var. ussuriense extract (CJE) on NO production, NK cell cytotoxicity and cytokine gene expressions related with macrophage and NK cell activity. Result : 1. CJE did not show any direct cytotoxic effects on 7250, HT1080, Hep G2 and CT-26 cells. 2. CJE activated macrophages partially to product NO and up-regulated gene expressions for iNOS in RAW 264.7 cells. 3. CJE promoted cytotoxicity of NK cells against YAC-1 cells at higher concentration than 200 ${\mu}g/ml$. 4. CJE up-regulated gene expressions for $IL-1{\beta}$, IL-2, iNOS, $IFN-{\gamma}$ and $TNF-{\alpha}$ in mice splenocytes.　５. CJE inhibited lung tumor metastasis induced by CT-26 cell transplantation compared with the control group.　Conclusion : It could be concluded that CJE is an effective herbal drug for immune modulating and anti-cancer treatment by promoting activity of macrophages and NK cells.

• The Journal of Internal Korean Medicine
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• v.24 no.2
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• pp.315-328
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• 2003

This study was performed to investigate the effect of Bunsimgieum on antitumor effect after sarcoma-180 cells transplantation into peritoneal cavity or left groin and immune responses on the depressed immunity induced by methotrexate in mice. The Bunsimgieum extract of 10mg/kg was orally administered 14 days for antitumor effects and 21 days for immune responses. 50% inhibitory concentration($IC_{50}$) of SUN-1, SUN-C4, and SUN-396 cancer cell, mean sunvival days and body weight of tumor bearing mice, and growth of tumor mass for antitumor effect; delayed type hypersentivity, hemagglutinin titer, hemolysis titer, rosette forming cells, natured killer cell activity, lymphocyte transformation, productivity of interleukin-2, and phagocytic activity for their immune responses were measured in ICR mice. Significance in antitumor effect is noted in the enlongation of mean life days and inhibition of tumor growth(p<0.01, respectively). Significance of immune responses is also noted in hemolysis titer, lymphocyte transfumotion, IL-2 productivity, phagocytic activity, and natural killer cell activity at E/T ratio 100:1(p<0.01, respectively). Significant in rosette cell formation was seen at dosage of 20mg/kg(p<0.01). However, Difference of body weight as antitumor effect, delayed type hypersensitivity, and hemagglutinin titer were not shown significantly. According to the above results, it could be suggested that Bunsimgieum has prominent antitumor and immunity enhancing effect.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.7
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• pp.2665-2669
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• 2015

CD4+CD25+regulatory T cells (Tregs) play a key role in regulation of immnue response and maintenance of self-tolerance. Studies have found Tregs could suppress tumor-specific T cell-mediated immune response and promote cancer progression. Depletion of Tregs can enhance antitumor immunity. Dendritic cells (DCs) are professional antigen-presenting cells and capable of activating antigen-specific immune responses, which make them ideal candidate for cancer immunotherapy. Now various DC vaccines are considered as effective treatment for cancers. The aim of this study was to evaluate variation of Tregs in BALB/C mice with hepatocellular carcinoma and investigate the interaction between tumor-derived Tregs, effector T cells (Teff) and splenic DCs. We found the percentages of Tregs/CD4+ in the peripheral blood of tumor-bearing mice were higher than in normal mice. Tumor-derived Tregs diminished the up-regulation of costimulatory molecule expression on splenic DCs, even in the presence of Teff cells and simultaneously inhibited IL-12 and $TNF-{\alpha}$ secretion by DCs.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.8
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• pp.3659-3665
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• 2014

To assess inhibition mechanisms of a Phellinus igniarius (PI) extract on cancer, C57BL/6 mice were orally treated with PI extractive after or before implanting H22 (hepatocellular carcinoma ) or B16 (melanoma) cells. Mice were orally gavaged with different doses of PI for 36 days 24h after introduction of H22 or B16 cells. Mice in another group were orally treated as above daily for 42 days and implanted with H22 cells on day 7. Then the T lymphocyte, antibody, cytokine, LAK, NK cell activity in spleen, tumor cell apoptosis status and tumor inhibition in related organs, as well as the expression of iNOS and PCNA in tumor tissue were examined. The PI extract could improve animal immunity as well as inhibit cancer cell growth and metastasis with a dose-response relationship. Notably, PI's regulation with the two kinds of tumor appeared to occur in different ways, since the antibody profile and tumor metastasis demonstrated variation between animals implanted with hepatocellular carcinoma and melanoma cells.

• Biomedical Science Letters
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• v.29 no.3
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• pp.178-183
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• 2023

Natural killer (NK) cells are innate cytotoxic lymphoid cells that actively prevent neoplastic development, growth, and metastatic dissemination in a process called cancer immunosurveillance. Regulation of the cytotoxic activity of NK cells relies on integrated interactions between inhibitory receptors and numerous activating receptors that act in tandem to eliminate tumor cells efficiently. Conventional chemotherapy is designed to produce an anti-proliferative or cytotoxic effect on early tumor cell division. Therapies designed to kill cancer cells and simultaneously maintain host anti-tumor immunity are attractive strategies for controlling tumor growth. Depending on the drug and dose used, several chemotherapeutic agents cause DNA damage and cancer cell death through apoptosis, immunogenic cell death, or other forms of non-killing (i.e., mitotic catastrophe, senescence, autophagy). Among stress-induced immunostimulatory proteins, changes in the expression levels of NK cell activating and inhibitory ligands and tumor cell death receptors play an important role in the detection and elimination by innate immune effectors including NK cells. Therefore, we will address how these cytotoxic lymphocytes sense and respond to high and low concentrations of drug-induced stress to the drug cisplatin, among the various types of drugs that contribute to their anticancer activity.

• CELLMED
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• v.3 no.1
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• pp.3.1-3.3
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• 2013

The receptor activator of NF-${\kappa}B$ ligand (RANKL), a member of the tumor necrosis factor ligand family, has extensive functions beyond osteoclast development. RANKL is expressed in many immune cells such as osteoblasts, osteocytes, marrow stromal cells, activated T cells, synovial cells, keratinocytes, and mammary gland epithelial cells as well as in various tissues. The ligation of RANK by RANKL promotes dendritic cells (DCs) survival through prosurvival signals and the up-regulation of the anti-apoptotic proteins Bcl-2 and Bcl-$x_L$ and plays a crucial role in DCs-mediated Th1 differentiation. Therefore, RANKL plays an important role in the regulation of DCs/T cells-mediated specific immunity. This review will briefly inform our current understanding of the role of RANKL signaling in T cells-DCs communication in the immune system.