• IMMUNE NETWORK
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• v.14 no.6
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• pp.277-288
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• 2014

T cells are central players in the regulation of adaptive immunity and immune tolerance. In the periphery, T cell differentiation for maturation and effector function is regulated by a number of factors. Various factors such as antigens, co-stimulation signals, and cytokines regulate T cell differentiation into functionally specialized effector and regulatory T cells. Other factors such as nutrients, micronutrients, nuclear hormones and microbial products provide important environmental cues for T cell differentiation. A mounting body of evidence indicates that the microbial metabolites short-chain fatty acids (SCFAs) have profound effects on T cells and directly and indirectly regulate their differentiation. We review the current status of our understanding of SCFA functions in regulation of peripheral T cell activity and discuss their impact on tissue inflammation.

• Korean Journal of Food Science and Technology
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• v.34 no.4
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• pp.694-699
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• 2002

The purpose of this study is to observe the effect of bovine colostral whey fractions on proliferation of Th1 cells and to verify the effect of whey fractions that are directly related to growth of Th1 cells on macrophages activation. Whey was fractionated into 3 fractions depending on by ultrafiltration (fraction (Fr.) I; molecular weight (Mw.) 10 kDa and more, Fr. II; Mw. $1\;kDa{\sim}10\;kDa$, Fr. III; Mw. less than 1 kDa) and examined by SDS-polyacrylamide gel electrophoresis. Fr. II stimulated and proliferated Th1 cells most at 1 mg/mL concentration and the percentage of cell proliferation was 67.1%. The secretive induction of tumor necrosis $factor-{\alpha}$ $(TNF-{\alpha})$ by whey, Fr. II, protein fraction (Fr. P) and oligosaccharide fraction (Fr. O) after fractionating Fr. II into Fr. P and Fr. O on the basis of Th1 cells growth was that Fr. O had more 80% secretive induction of $TNF-{\alpha}$ than that of $1\;{\mu}g/mL$ lipopolysaccharide that was positive control. So confirmed that Fr. O induced $TNF-{\alpha}$ secretion by activating macrophages.

• Journal of Microbiology and Biotechnology
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• v.28 no.1
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• pp.65-76
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• 2018

Although there has been a steady increase in the prevalence of food allergies worldwide in recent decades, no effective therapeutic strategies have been developed. Modulation of the gut microbiota composition and/or function through probiotics has been highlighted as a promising target for protection against food allergies. In this study, we aimed to investigate the allergy-reducing effects of a probiotic mixture (P5: Lactococcus lactis KF140, Pediococcus pentosaceus KF159, Lactobacillus pentosus KF340, Lactobacillus paracasei 698, and Bacillus amyloliquefaciens 26N) in mice with ovalbumin (OVA)-induced food allergy. Administration of P5 significantly suppressed the oral OVA challenge-induced anaphylactic response and rectal temperature decline, and reduced diarrhea symptoms. Moreover, P5 also significantly inhibited the secretion of IgE, Th2 cytokines (interleukin (IL)-4, IL-5, IL-10, and IL-13), and Th17 cytokines (IL-17), which were increased in mice with OVA-induced food allergy, and induced generation of CD4+Foxp3+ regulatory T cells. These results revealed that P5 may have applications as a preventive agent against food allergy.

• 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.21 no.6
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• pp.43.1-43.14
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• 2021

Group 3 innate lymphoid cells (ILC3), which express IL-22 and IL-17A, has been introduced as one of pathologic cells in axial spondyloarthritis (axSpA). Dyslipidaemia should be managed in axSpA patients to reduce cardiovascular disease, and dyslipidaemia promotes inflammation. This study aimed to reveal the role of circulating ILC3 in axSpA and the impact of dyslipidaemia on axSpA pathogenesis. AxSpA patients with or without dyslipidaemia and healthy control were recruited. Peripheral blood samples were collected, and flow cytometry analysis of circulating ILC3 and CD4⁺ T cells was performed. The correlation between Ankylosing Spondylitis Disease Activity Score (ASDAS)-C-reactive protein (CRP) and circulating immune cells was evaluated. The effect of oxidized low-density lipoprotein cholesterol (oxLDL-C) on immune cell differentiation was confirmed. AxSpA human monocytes were cultured with with oxLDL-C, IL-22, or oxLDL-C plus IL-22 to evaluate osteoclastogenesis using tartrate-resistant acid phosphatase (TRAP) staining and real-time quantitative PCR of osteoclast-related gene expression. Total of 34 axSpA patients (13 with dyslipidaemia and 21 without) were included in the analysis. Circulating IL-22⁺ ILC3 and Th17 were significantly elevated in axSpA patients with dyslipidaemia (p=0.001 and p=0.034, respectively), and circulating IL-22⁺ ILC3 significantly correlated with ASDAS-CRP (Rho=0.4198 and p=0.0367). Stimulation with oxLDL-C significantly increased IL-22⁺ ILC3, NKp44^- ILC3, and Th17 cells, and these were reversed by CD36 blocking agent. IL-22 and oxLDL-C increased TRAP⁺ cells and osteoclast-related gene expression. This study suggested potential role of circulating IL-22⁺ ILC3 as biomarker in axSpA. Furthermore, dyslipidaemia augmented IL-22⁺ ILC3 differentiation, and oxLDL-C and IL-22 markedly increased osteoclastogenesis of axSpA.

• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.5
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• pp.1330-1334
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• 2003

Astragali Radix(AR), one of the strong tonic herbs, is known to improve immunological responses in mice and human. In this study, AR's ai-reinforcing effect was examined in the context of CD4/sup +/ T cells' TCR/CD3 induced activation responses. In order to evaluate the direct effect of AR on helper T cells, CD4/sup +/ T cells are isolated using magnetic bead and their proliferation and CD69 expression in AR treated medium were assessed with anti-CD3/anti-CD28 activation for 48h. CD4 T cells' proliferation was slightly increased but there was little effect on CD69 expression. RT PCR and ELISA equally demonstrated that IL-2 and IL-4 production was increased but IFN-ν was down-regulated. This shows AR ethanol extract favors Th2 cytokine profile under neutral conditions.

• The Journal of the Korean Society for Microbiology
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• v.17 no.1
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• pp.7-14
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• 1982

A model of induction of neoplasia by viruses has develpoed from experimental studies in animals and in cultured cells and oncogenic transformation of cells is the result of integration of viral genetic information into the cellular DNA. The evidence for these associations was derived primarily from seroepidemiologic investigation. However, data indicating that the relation between HSV-2 and cervical cancer fits the model derived from experimental animal studies are not yet sufficient to draw conclusion with regard to the etiologic role the virus in the development of the neoplasms. In other hand, the K562 tumor cell is highly susceptible target for natural killer cell lysis by the lymphocytes of human and murine periperal blood. The characteristics of this effector cell type has been investigated. A study on natural killer cell mediated cytotoxicity(NKMC) against $^{51}Cr$-K562 as target cell was studed in HSV-2 infected ICR mouse. We have studied for susceptibility of HSV-2 against mouse embryo fibroblast(MEF) cells and NKMC from HSV-2 infected mouse. The results obtained that the mouse embryo fibroblast cells culture, the number and size of the cells were markedly increased and formed a monolayers relatively rapid, and become complete monolayer sheet around 72 hrs. Duration of cytopathic effect on MEF cells was rapid by serial passing of HSV-2. The morphology of the HSV-2 infected cells appear to be mainly round, ovium, spindle form and some of them was forming large giant cells. The NKMC was decrease in mouse with HSV-2 and comparison between effector/target cells ratio as 25:1 and 50:1 respectively, the NKMC was found to be more significantly decreased than normal control we have concluded that the natural killer cell activity of the viral infected mouse was shown as a suppressed during the HSV-2 infection, day 7th and 14th.

• Journal of the Korean Institute of Electrical and Electronic Material Engineers
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• v.17 no.11
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• pp.1224-1229
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• 2004

The purpose of this study is to research and develop tin oxide-flyash composite for lithium Ion polymer battery. Tin oxide is one of the promising material as a electrode active material for lithium Ion polymer battery (LIPB). Tin-based oxides have theoretical volumetric and gravimetric capacities that are four and two times that of carbon, respectively. We investigated cyclic voltammetry, AC impedance and charge/discharge cycling of SnO$_2$-flyash/SPE/Li cells. The first discharge capacity of SnO$_2$-flyash composite anode was 639 mAh/g. The discharge capacity of SnO$_2$-flyash composite anode was 563 and 472 mAh/g at 6th and 15th cycle, respectively. The SnO$_2$-flyash composite anode with PVDF-PMMA-PC-EC-LiClO$_4$ electrolyte showed good capacity with cycling.

• Nutrition Research and Practice
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• v.15 no.6
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• pp.673-685
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• 2021

BACKGROUND/OBJECTIVES: Obesity is associated with the impaired regulation of T cells characterized by increased numbers of Th1 and Th17 cells and the dysregulation of vitamin D metabolism. Both obesity and vitamin D have been reported to affect autophagy; however, a limited number of studies have investigated the effects of vitamin D on T cell autophagy in obese mice. Therefore, we aimed to determine whether in vitro treatment with vitamin D affects the proliferation, function, and autophagy of T cells from obese and control mice. MATERIALS/METHODS: Five-week-old male C57BL/6 mice were fed control or high-fat diets (10% or 45% kcal fat: CON or HFDs, respectively) for 12 weeks. Purified T cells were stimulated with anti-CD3 and anti-CD28 monoclonal antibodies and cultured with either 10 nM 1,25(OH)₂D₃ or 0.1% ethanol (vehicle control). The proliferative response; expression of CD25, Foxp3, RORγt, and autophagy-related proteins (LC3A/B, SQSTM1/P62, BECLIN-1, ATG12); and the production of interferon (IFN)-γ, interleukin (IL)-4, IL-17A, and IL-10 by T cells were measured. RESULTS: Compared with the CON group, T cell proliferation tended to be lower, and the production of IFN-γ was higher in the HFD group. IL-17A production was reduced by 1,25(OH)2D₃ treatment in both groups. The LC3 II/I ratio was higher in the HFD group than the CON group, but P62 did not differ. We observed no effect of vitamin D treatment on T cell autophagy. CONCLUSIONS: Our findings suggest that diet-induced obesity may impair the function and inhibit autophagy of T cells, possibly leading to the dysregulation of T cell homeostasis, which may be behind the aggravation of inflammation commonly observed in obesity.

• Food Science and Biotechnology
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• v.17 no.3
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• pp.631-636
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• 2008

Acanthopanax divaricatus var. albeofructus (ADA) have been shown to have various levels of activity such as antioxidant, anticancer, antivirus, and immunostimulatory effects. However, little is known about its mechanism related to the modulation of immune activities. In this study, a water extract of ADA leaves were used to treat human peripheral blood mononuclear cells (hPBMC) to determine the underlying mechanisms for the immunostimulatory effects. To characterize its immunomodulatory activity, the secretion level of various cytokines including IL-2, IL-4, IL-6, IL-10, IL-12, IFN-$\gamma$, and TNF-$\alpha$ were measured using enzyme-linked immunosorbent assay (ELISA). Treatment of hPBMC with ADA leaf extract in an in vitro experiment induced various Th1 cytokines in a dose-dependent manner. A significant increase of IL-2, IL-12, IFN-$\gamma$, and TNF-$\alpha$ secretion was observed in the presence of ADA leaf extract. In contrast, Th2 cytokines including IL-4 and IL-6 were suppressed. There was no significant change in IL-10 release. Our results showed an increase in Th1 and a decrease in Th2 cytokine secretion which suggests that ADA may influence the immune response towards a predominance of Th1 cytokines in the immune system.