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Immune network : official journal of the Korean as... 6건

  1. [국내논문]   Peripheral Generation of $CD4^+CD25^+Foxp3^+$ Regulatory T Cells  

    Kim, Byung-Seok (Laboratory of Immunology, Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University ) , Park, Young-Jun (Laboratory of Immunology, Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University ) , Kang, Chang-Yuil (Laboratory of Immunology, Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University)
    Immune network : official journal of the Korean association of immunobiologists v.7 no.1 ,pp. 1 - 9 , 2007 , 1598-2629 ,

    초록

    [ $CD4^+CD25^+$ ] regulatory T cells (Tregs) expressing the lineage-specific marker Foxp3 represent an important regulatory T cell that is essential for maintaining peripheral tolerance. Although it was believed that Treg development is solely dependent on the thymus, accumulating evidence demonstrates that Tregs can also be induced in the periphery. Considering the various origins of peripherally developed $CD4^+CD25^+Foxp3^+$ regulatory T cells, it seems likely that multiple factors are involved in the peripheral generation of Tregs.

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  2. [국내논문]   Th17과 자가면역 관절염  

    조미라 (가톨릭대학교 의과대학 류마티스연구센터 ) , 허유정 (가톨릭대학교 의과대학 류마티스연구센터 ) , 박진실 (가톨릭대학교 의과대학 류마티스연구센터 ) , 이선영 (가톨릭대학교 의과대학 류마티스연구센터 ) , 성영철 (포항공과대학 생명과학과 ) , 김호연 (가톨릭대학교 의과대학 류마티스연구센터)
    Immune network : official journal of the Korean association of immunobiologists v.7 no.1 ,pp. 10 - 17 , 2007 , 1598-2629 ,

    초록

    Autoimmune arthritis, such as rheumatoid arthritis (RA), is a chronic inflammatory disorder that primarily affects the joints and then results in their progressive destruction. Effector Th cells have been classified as Th1 and Th2 subsets based on their cytokine expression profiles and immune regulatory function. Another subset of T cells termed Th17 was recendy discovered and known to selectively produce IL-17. Also, Th17 was shown to be generated by TGF ${\beta}$ and IL-6 and maintained by IL-23. IL-17 is a proinflammatory cytokine that is considered to involve the development of various inflammatory autoimmune diseases such as RA, asthma, lupus, and allograft rejection. IL-17 is present in the sera, synovial fluids and synovial biopsies of most RA patient. IL-17 activates RA synovial fibroblasts to synthesize IL-6, IL-8 and VEGF via PI3K/Akt and NF- ${\kappa}B$ dependent pathway. IL-17 increases IL-6 production, collagen destruction and collagen synthesis. In addition, it not only causes bone resorption but also increases osteoclastogenesis and fetal cartilage destruction. Inhibition of the IL-17 production may contribute a novel therapeutic approach along with potent anti-inflammatory effect and with less immunosuppressive effect on host defenses.

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  3. [국내논문]   Dexamethasone Does Not Inhibit Airway CXC Chemokine Expression and Neutrophilia in a Murine Model of Asthma - Mechanism of Steroid Resistance in Asthma  

    Lee, Young-Man (Department of Immunology, Chonbuk National University Medical School ) , Kang, Nam-In (Department of Immunology, Chonbuk National University Medical School ) , Lee, Hern-Ku (Department of Immunology, Chonbuk National University Medical School)
    Immune network : official journal of the Korean association of immunobiologists v.7 no.1 ,pp. 18 - 25 , 2007 , 1598-2629 ,

    초록

    Background: Although glucocorticoids (GCs) are effective in controlling asthma in the majority of patients, a subset of asthmatics fails to demonstrate a satisfactory response, even to systemic GC therapy. This population is referred to as being "steroid-resistant". The actual mechanism underlying steroid resistance in asthma remains to be elucidated. Methods: We have investigated how dexamethasone (DEX) regulates asthmatic phenotypes in a murine model of asthma, in which mice received i.p. immunization twice, followed by two bronchoprovocations with aerosolized OVA with a one-week interval, which we have recently described. Results: Pretreatment with DEX resulted in an inhibition of NF- ${\kappa}B$ activation in asthmatic lungs, and also inhibited bronchoalveolar lavage (BAL) levels of NF- ${\kappa}B$ -dependent cytokines such as TNF- ${\alpha}$ and CC chemokines [eotaxin and monocyte chemotactic protein (MCP)-1]. DEX was effective in suppressing airway hyperresponsiveness (AHR) at 10 h, Th2-dependent asthmatic phenotypes such as airway eosinophilia, BAL levels of Th2 cytokines (IL-5 and IL-13), and mucin production. However, DEX failed to suppress BAL levels of CXC chemokines [macrophage inflammatory protein-2 (MIP-2) and keratinocyte-derived chemokine (KC)] and airway neutrophilia. Conclusion: Airway neutrophilia is among the phenomena observed in patients with severe GC-resistant asthma. This study will provide insight into the molecular basis for airway neutrophila seen in steroid-resistant asthma. Further studies are required to delineate the underlying mechanism of CXC chemokine expression in asthma.

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  4. [국내논문]   결핵균 단백항원 자극에 의한 대식세포의 TNF-${\alpha}$ 및 IL-6 생성과 ERK 활성화  

    안혜정 (연세대학교 의과대학 미생물학교실 ) , 조상래 (연세대학교 의과대학 미생물학교실 ) , 백태현 (건양대학교 의과대학 미생물학교실 ) , 이정림 (건양대학교 의과대학 미생물학교실 ) , 최인홍 (연세대학교 의과대학 미생물학교실)
    Immune network : official journal of the Korean association of immunobiologists v.7 no.1 ,pp. 26 - 30 , 2007 , 1598-2629 ,

    초록

    Background: Mycobacterial antigens released as PIM, LM, LAM, lipoproteins and other cellular factors may contribute to macrophage and dendritic cell activation through pattern recognition receptors such as TLRs. In this study, we assessed cytokine production and ERK activation with stimulation of several major mycobacterial antigens. Methods: Purified mycobacterial antigens (10, 22, 30, 38kDa) and recombinant antigens (6, 16, 19, 38kDa, Ag85A antigen) were studied. The production of cytokines (TNF- ${\alpha}$ , IL-12, IL-6) was measured by ELISA. The ERK activation was detected by western blotting. The expression of TLR2 or TLR4 was measured by flow cytometry. Results: Among purified antigens only 30kDa antigen induced production of IL-6 or TNF- ${\alpha}$ in THP-1 macrophage cells. When THP-1 macrophage cells were treated with 30kDa antigen, phosphorylation of ERK was detected. ERK activation also occurred in TLR2 transfectant HEK293 cells with 30kDa antigen stimulation. Conclusion: 30kDa antigen is one of the major mycobacterial antigens inducing cytokine production and MAP kinases phosphorylation in macrophages.

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  5. [국내논문]   Mizoribine Inhibits Production of Pro-inflammatory Cytokines and $PGE_2$ in Macrophages  

    Han, Shin-Ha (Department of Pharmacy, Sahmyook University ) , Kim, Kwang-Hee (Department of Pharmacy, Sahmyook University ) , Kim, Hyun-Yul (Department of Pharmacy, Sahmyook University ) , Kwon, Jeung-Hak (Department of Pharmacy, Sahmyook University ) , Han, Nam-Joo (Department of Pharmacy, Sahmyook University ) , Lee, Chong-Kil (College of Pharmacy, Chungbuk National University ) , Kim, Kyung-Jae (Department of Pharmacy, Sahmyook University)
    Immune network : official journal of the Korean association of immunobiologists v.7 no.1 ,pp. 31 - 38 , 2007 , 1598-2629 ,

    초록

    Background: Mizoribine (MZR) is an imidazole nucleoside isolated from Eupenicillium brefeldianum. MZR is currendy in clinical use for patients who have undergone renal transplantation. Therapeutic efficacy of MZR has also been demonstrated in rheumatoid arthritis and lupus nephritis. MZR has been shown to inhibit the proliferation or lymphocytes by interfering with inosine monophosphate dehydrogenase. Since the exact mechanism by which MZR benefits rheumatoid arthritis (RA) is not clear, we investigated the ability of MZR to direct its immunosuppressive influences on other antigen presenting cells, such as macrophages. Methods: Mouse macrophage RAW264.7 cells were stimulated with lipopolysaccharide in the presence of MZR. To elucidate the mechanism of the therapeutic efficacy in chronic inflammatory diseases, we examined the effects of MZR on the production of pro-inflammatory cytokines, nitric oxide (NO) and prostaglandin $E_2\;(PGE_2)$ in macrophages. Results: MZR dose-dependendy decreased the production of nitric oxide and pro- inflammatory cytokines such as tumor necrosis factor- ${\alpha}$ (TNF- ${\alpha}$ ), interleukins $1{\beta}$ (IL- ${\beta}$ and IL-6 $PGE_2$ . Examination of gene expression levels showed that the anti-inflammatory effect correlated with the down-regulation of inducible nitiric oxide synthase expression, cycloxygenase-2 expression and TNF- ${\alpha}$ gene expression. Conclusion: In this work, we resulted whether MZR $(1.25{\sim}10{\mu}g/ml)$ inhibited macrophage activation by inhibiting secretion of pro-inflammatory cytokines, NO and $PGE_2$ . These findings provide an explanation for the therapeutic efficacy of MZR in chronic inflammation-associated diseases.

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  6. [국내논문]   류마티스관절염 활막세포에서 NF-${\kappa}B$ 신호전달을 통한 MIF의 SDF-1 생성 유도  

    조미라 (가톨릭대학교 의과대학 류마티스연구센터 ) , 박미경 (가톨릭대학교 의과대학 류마티스연구센터 ) , 김경운 (가톨릭대학교 의과대학 류마티스연구센터 ) , 오혜좌 (가톨릭대학교 의과대학 류마티스연구센터 ) , 이선영 (가톨릭대학교 의과대학 류마티스연구센터 ) , 박진실 (가톨릭대학교 의과대학 류마티스연구센터 ) , 허유정 (가톨릭대학교 의과대학 류마티스연구센터 ) , 주지현 (가톨릭대학교 의과대학 류마티스연구센터 ) , 민준기 (가톨릭대학교 의과대학 류마티스연구센터 ) , 이상헌 (건국대학교 의과대학 내과학교실 ) , 박성환 (가톨릭대학교 의과대학 류마티스연구센터 ) , 김호연 (가톨릭대학교 의과대학 류마티스연구센터)
    Immune network : official journal of the Korean association of immunobiologists v.7 no.1 ,pp. 39 - 47 , 2007 , 1598-2629 ,

    초록

    Background: Stromal cell-derived factor (SDF)-1 is a potent chemoattractant for activated T cells into the inflamed Rheumatoid arthritis (RA) synovium. To determine the effect of macrophage migration inhibitory factor (MIF) on the production of SDF-1 in the inflamed RA synovium. Methods: The expression of SDF-1 and MIF in RA and Osteoarthritis (OA) synovium was examined by immunohistochemical staining. The SDF-1 was quantified by RT-PCR and ELISA after RA fibroblast like synoviocyte (FLS) were treated with MIF in the presence and absence of inhibitors of intracellular signal molecules. The synovial fluid (SF) and serum levels of MIF and SDF-1 in RA, OA and healthy control were measured by ELISA. Results: Expression of SDF-1 and MIF in synovium was higher in RA patients than in OA patients. The production of SDF-1 was enhanced in RA FLS by MIF stimulation. Such effect of MIF was blocked by the inhibitors of NF- ${\kappa}B$ . Concentrations of SDF-1 in the serum and SF were higher in RA patients than in OA patients and healthy control. SDF-1 and MIF was overexpressed in RA FLS, and MIF could up-regulate the production of SDF-1 in RA FLS via NF- ${\kappa}B$ -mediated pathways. Conclusion: These results suggest that an inhibition of interaction between MIF from T cells and SDF-1 of FLS may provide a new therapeutic approach in the treatment of RA.

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