• IMMUNE NETWORK
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• 제23권1호
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• pp.4.1-4.15
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• 2023

Th cells, which orchestrate immune responses to various pathogens, differentiate from naive CD4 T cells into several subsets that stimulate and regulate immune responses against various types of pathogens, as well as a variety of immune-related diseases. Decades of research have revealed that the fate decision processes are controlled by cytokines, cytokine receptor signaling, and master transcription factors that drive the differentiation programs. Since the Th1 and Th2 paradigm was proposed, many subsets have been added to the list. In this review, I will summarize these events, including the fate decision processes, subset functions, transcriptional regulation, metabolic regulation, and plasticity and heterogeneity. I will also introduce current topics of interest.

• 한국수의병리학회지
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• 제3권1호
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• pp.15-25
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• 1999

To elucidate the mechanism of age-related development in FGS/NgaKIST mice with spontaneous glomerulosclerotic lesion, we examined expression and localization of various cytokine mRNA in the kidney in the progression of diseases. This mouse model is the first to develop spontanously occuring glomerosclerotic lesion in the kidney. In this study, we detected the up-regulation of local cytokine genes such as IL-1$\beta$, IL-2, IL-6, IL-10, TNF-$\alpha$, TGF-$\beta$, and IFN- $\gamma$ in the kidneys. In RT-PCR and Southern blot analysis, we detected gradual expressions of cytokine mRNA of IL-1$\beta$, IL-2, IL-6, IFN- $\gamma$, and TNF $\alpha$ mRNA during the course of disease. Other cytokines including IL -10 and TGF -$\beta$ were found to be appeared the slightly expressed level at 3 to 12 weeks before onset of inflammatory lesion but they are highly expressed at the end-stage of the disease accompaning high proteinurea and wasting. In situ RT-PCR, each cytokine mRNA were specifically localized in a variety of cells including mesangial, endothelial, parietal epithelial, tubular epithelial, arterial muscle cell, and infiltrated inflammatory cells. In addition, TNF - $\alpha$was detected moderately in the visceral and parietal epithelial cell, but weakly in endothelial and mesangial cells, whereas IL-1 $\beta$ and IL -6 were strong in mesangial regions. IL-6 and TNF- $\alpha$ was highly localized in the damaged proximal and collecting tubules. Especially, TGF -$\beta$ mRNA was highly found in mesangial cells within glomerulus and interstitium during the end-stage of this disease.. These results indicate that pro inflammatory cytokines such as IL-1 $\beta$, IL-2, IL-6, and TNF- $\alpha$ were gradually expressed from the early stage of this disease to the end-stage, and that IL-10 and TGF-$\beta$ may be important in the accumulation of extracellular matrix(ECM) within glomerulus and periglomerular fibrosis in the progression of this disease as well as tissue destruction in end-stage of this disease.

• IMMUNE NETWORK
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• 제7권2호
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• pp.66-74
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• 2007

Background: The genus Flavivirus consists of many emerging arboviruses, including Dengue virus (DV), Japanese encephalitis virus (JEV) and West Nile virus (WNV). Effective preventive vaccines remain elusive for these diseases. Mice are being increasingly used as the animal model for vaccine studies. However, the pathogenic mechanisms of these viruses are not clearly understood. Here, we investigated the interaction of DV and JEV with murine bone marrow-derived dendritic cells (bmDC). Methods: ELISA and FACS analysis were employed to investigate cytokine production and phenotypic changes of DCs obtained from bone marrow following flavivirus infection. Results: We observed that these viruses altered the cytokine profile and phenotypic markers. Although both viruses belong to the same family, JEV-infected bmDC produced anti-inflammatory cytokine (IL-10) along with pro-inflammatory cytokines, whereas DV infection induced production of large amounts of pro-inflammatory cytokines (IL-6 and TNF-${\alpha}$) and no IL-10 from murine bmDCs. Both flaviviruses also up-regulated the expression of co-stimulatory molecules such as CD40, CD80 and CD86. JEV infection led to down-regulation of MHC II expression on infected bmDCs. We also found that cytokine production induced by JEV and DV is MyD88-dependent. This dependence was complete for DV, as cytokine production was completely abolished in the absence of MyD88. With regard to JEV, the absence of MyD88 led to a partial reduction in cytokine levels. Conclusion: Here, we demonstrate that MyD88 plays an important role in the pathogenesis of flaviviruses. Our study provides insight into the pathogenesis of JEV and DV in the murine model.

• 생명과학회지
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• 제32권11호
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• pp.899-907
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• 2022

Quercetin은 과일과 채소에 풍부한 플라보노이드 중의 하나로써, 항산화, 항염증, 항암, 항바이러스 활성 등 다양한 약리학적 활성을 가지고 있는 것으로 알려져 있다. 본 연구에서는 in vitro 모델에서 quercetin의 항염증 활성과 작용기전을 연구하였다. Quercetin은 LPS로 자극된 RAW264.7에서 세포 생존율에 영향 없이 NO 생산을 농도 의존적으로 저해하였고, iNOS와 COX-2 단백질의 발현을 억제하였다. 게다가, quercetin은 LPS로 유도된 p38, JNK, ERK의 인산화를 농도 의존적으로 저해하였고, NF-κB p65 단백질과 억제자인 IκBα 단백질의 인산화를 저해하였다. 이러한 결과는 quercetin의 항염증 활성이 MAPK 경로와 NF-κB를 조절함으로써 이루어진다는 것을 시사한다. Quercetin에 의해 4종류의 친 염증성 cytokine (CSF2, IL-1β, IL-6, TNF-α)의 발현 변화를 정량적 real-time PCR 방법으로 확인한 결과, 모든 cytokine 유전자의 발현이 감소됨을 확인하였다. 종합적으로, 본 연구결과는 플라보노이드 quercetin이 RAW264.7 세포에서 LPS로 유도된 염증반응을 MAPK 경로와 NF-κB경로를 통해 억제하고 친염증성 cytokine 유전자의 발현을 억제함으 로써 조절한다는 것을 제시한다.

• BMB Reports
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• 제48권2호
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• pp.103-108
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• 2015

Trichomoniasis caused by the parasitic protozoan Trichomonas vaginalis is the most common sexually transmitted disease in the world. Dendritic cells are antigen presenting cells that initiate immune responses by directing the activation and differentiation of naive T cells. In this study, we analyzed the effect of Trichomonas vaginalis-derived Secretory Products on the differentiation and function of dendritic cells. Differentiation of bone marrow-derived dendritic cells in the presence of T. vaginalis-derived Secretory Products resulted in inhibition of lipopolysaccharide-induced maturation of dendritic cells, down-regulation of IL-12, and up-regulation of IL-10. The protein components of T. vaginalis-derived Secretory Products were shown to be responsible for altered function of bone marrow-derived dendritic cells. Chromatin immunoprecipitation assay demonstrated that IL-12 expression was regulated at the chromatin level in T. vaginalis-derived Secretory Products-treated dendritic cells. Our results demonstrated that T. vaginalis- derived Secretory Products modulate the maturation and cytokine production of dendritic cells leading to immune tolerance.

• 동의생리병리학회지
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• 제26권6호
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• pp.823-833
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• 2012

Now a days, number of non alcoholic fatty liver patients are increasing more rapidly compare to past rate, and the average age of patients is getting younger, but there are no appropriate therapeutics in non alcoholic fatty liver disease. This study was aimed to analyze relationship between non alcoholic fatty liver disease and Injinho-tang. The papers were collected and analysed from domestic and international journals. The effects of Injinho-tang and constituent-herb were researched. Non-alcoholic fatty liver disease was induced complex causes of the metabolic syndrome. Medications that can be used in non-alcoholic fatty liver disease, it should be have many effects such as anti-hepatic fibrosis, hepatocyte protection, liver cancer inhibitory effect, inflammatory cytokine regulation, improving hyperlipidemia, weight control, decrease the toxicity of the drug, antioxidant. Injinho-tang (Artemisia capillaris Thunb, Gardenia fructus, Rhei rhizome) has been widely used in disease that causes jaundice and liver biliary disease. Drugs for standardization of Injinho-tang index components(6,7-Dimethylesculetin, geniposide, rhein) have been presented. And Injinho-tang has been proven reliability in the administration of single dose toxicity. Also clinical stability in the administration of four years was reported. Injinho-tang has been reported some effects which anti-hepatic fibrosis, hepatocyte protection, liver cancer inhibitor, inflammatory cytokine regulation, improving hyperlipidemia, weight control, decrease the toxicity of the drug, and antioxidant. Therefore, Injinho-tang can be used in Non alcoholic fatty liver disease without Syndrome Differentiation.

• IMMUNE NETWORK
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• 제15권3호
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• pp.135-141
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• 2015

Dysfunction of gut immune regulation is involved in mucosal damage in inflammatory bowel disease (IBD). However, there is still no efficacious immune-regulator for the treatment of IBD. Alloferon is a novel immune-modulatory peptide that was originally isolated from infected insects. It shows anti-inflammatory effects by the regulation of cytokine production by immune cells and their activities. Therefore, we investigated the effect of alloferon in a mouse model of colitis using dextran sulfate sodium (DSS). Colitis was induced by administration of DSS in drinking water for 7 consecutive days. It was confirmed by the presence of weight loss, diarrhea, hematochezia, and colon contraction. Alloferon was injected 4 days after DSS administration. We found that alloferon improved the pathogenesis of IBD based on the reduced disease activity index (DAI) and colon contraction. Edema, epithelial erosion, and immune cell infiltration were found in mice administered DSS, but the phenomena were reduced following alloferon treatment. The plasma level of IL-6, a classical pro-inflammatory cytokine in colitis, was also decreased by alloferon. Moreover, alloferon inhibited the TNF-${\alpha}$-induced degradation and phosphorylation of $I{\kappa}B$ in Colo205 colon cancer cells. Taken together, these results show that alloferon has anti-inflammatory effects and attenuates DSS-induced colitis.

• 혜화의학회지
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• 제17권2호
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• pp.167-183
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• 2008

KCSYJT medicines controlled $CD4^+/IFN-\gamma$, and $CD4^+/CD25^+/foxp3^+$ revelation that an experiment that motive allergy immune reponse because an in vitro experiment stimulates T cells of a NC/Nga mouse same time by anti-CD40/rmIL-4, and interleukin-$1{\beta}$, IL-6, TNF-$\alpha$, and TGF-$\beta$ mRNA outturn that bear in T and B cells decreased remarkably by KCSYJT medicines. Intracellular staining of splenocytes anti-CD40/rmIL-4 plus rmIL-4 stimulated as described in a, assessed after 24 h, KCSYJT exerts a mainly immunosuppressive effect that acts at least partially through suppression of the transcription factor GATA3 expression in $CD4^+$ T cells. We found that skin lesions, which were clinically and histologically very similar to human AD, mite antigen-induced dermatitis on the face, neck, ears and dorsal skin of inbred NC/Nga mice. Result that Th1 cell and Th2 cell observe to be shifted by cytokine expression with GATA3 regulation by KCSYJT medicines could know that KCSYJT medicines can use usefully in allergy autoimmnune diease.

• Asian Pacific Journal of Cancer Prevention
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• 제15권19호
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• pp.8469-8474
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• 2014

Introduction: Recent studies have indicated that down-regulation of the suppressor of cytokine signaling-1 (SOCS-1) gene results in tumor formation and that SOCS-1 acts as a tumor suppressor gene. SOCS-1 has been also suggested to function as a tumor suppressor with colorectal cancer. Objectives: In the present study, we aimed to determine the association of SOCS-1 expression in colorectal cancer tissues with clinicopathologic characteristics immunohistochemically and also to identify its prognostic significance. Materials and Methods: SOCS-1 expression was studied immunohistochemically in 67 patients diagnosed with resected colorectal carcinomas and 30 control subjects. Results: SOCS-1 expression was found in 46.3% of tumor tissues and 46.7% of the control group. Statistical analyses did not establish any significant association between SOCS-1 expression and clinicopathologic characteristics. Also, no significant association with SOCS-1 expression was found using progression-free survival and overall survival analyses (p=0.326 and p=0.360, respectively). Conclusions: Our results show that SOCS-1 has no prognostic significance in colorectal cancer.

• Molecular & Cellular Toxicology
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• 제1권2호
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• pp.124-129
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• 2005

Pro-inflammatory cytokines, such as tumor necrosis factor $(TNF)-{\alpha}$, interleukin-12 (IL-12) and interleukin $(IL-1)-{\beta}$, play a key role in causing inflammatory diseases, which are rheumatoid arthritis, Crohn's disease and sepsis. Accumulating evidences suggest that low level laser irradiation (LLLI) may have an anti-inflammatory action. However, there are few data regarding down regulation of Th1 immune response by using the diod typed laser emitting device for human patients. As a fundamental step in order to address this issue, we investigated immunological impact of the low level laser irradiation (10 mw laser diode with a wavelength of 630 nm) on expression of pro-inflammatory cytokines in murine immunocytes (splenocytes and peritoneal macrophages) in vitro. The LLLI on lipopolysaccharide (LPS 100 ng/ml)-stimulated murine splenocytes and macrophages, clearly down regulated mRNA expression of $TNF-{\alpha}$ and IL-12 in dose-dependent manner. In addition, LLLI significantly inhibits the NO production in the LPS-stimulated murine macrophages. This data suggests that LLLI (wavelength of 630 nm) may exert an anti-inflammatory action via modulation of pro-inflammatory cytokine and NO production pathway.