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콜라겐으로 경구 관용을 유도한 관절염 동물 모델의 세포 특이적 면역 반응 조사
민소연,황수연,이재선,김주영,이강은,김경운,김영훈,도주호,김호연,Min, So-Youn,Hwang, Sue-Yun,Lee, Jae-sun,Kim, Ju-Young,Lee, Kang-Eun,Kim, Kyung-Wun,Kim, Young-Hun,Do, Ju-Ho,Kim, Ho-Youn 대한면역학회 2003 Immune Network Vol.3 No.2
Oral administration of antigen has long been considered as a promising alternative for the treatment of chronic autoimmune diseases including rheumatoid arthritis (RA), and oral application of type II collagen (CII) has been proven to improve pathogenic symptoms in RA patients without problematic side effects. To further current understandings about the immune suppression mechanisms mediated by orally administered antigens, we examined the changes in IgG subtypes, T-cell proliferative response, and proportion of interleukin (IL)-10 producing Th subsets in a time course study of collagen induced arthritis (CIA) animal models. We found that joint inflammation in CIA mouse peaked at 5 weeks after first immunization with CII, which was significantly subdued in mice pre-treated by repeated oral administration of CII. Orally tolerized mice also showed increase in their serum level of IgG1, while the level of IgG2a was decreased. T-cell proliferation upon CII stimulation was also suppressed in lymph nodes of mice given oral administration of CII compared to non-tolerized controls. When cultured in vitro in the presence of CII, T-cells isolated from orally tolerized mice presented higher proportion of $CD4^+IL-10^+$ subsets compared to non-tolerized controls. Interestingly, such increase in IL-10 producing cells were obvious first in Peyer's patch, then by 5 weeks after immunization, in mesenteric lymph node and spleen instead. This result indicates that a particular subset of T-cells with immune suppressive functions might have migrated from the original contact site with CII to inflamed joints via peripheral blood after 5 weeks post immunization.
류마티스 질환에서 혈청 Soluble Fas Ligand (sFasL), FasL-Fas 복합체, FasL-IgG 복합체 측정
민준기 ( Jun Ki Min ),민소연 ( So Youn Min ),조미라 ( Mi Ra Cho ),정재연 ( Jae Yeon Jeong ),주대명 ( Dae Myung Jue ),민도준 ( Do June Min ),조철수 ( Chul Soo Cho ),김호연 ( Ho Youn Kim ) 대한류마티스학회 2000 대한류마티스학회지 Vol.7 No.4
Objective: To quantify the soluble Fas ligand (sFasL) and to measure FasL-Fas complex and FasL-IgG complex in the sera of patients with various rheumatic diseases: systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), systemic sclerosis (SSc), and adult onset Still`s disease (AOSD). Methods: Serum samples were obtained from 37 patients with SLE, 40 with RA, 30 with SSc, 20 with AOSD, and 40 healthy controls. The serum sFasL, FasL-Fas complex, and FasL-IgG complex were measured using a sandwich enzyme-linked immunoabsorbent assay. Hospital medical records were retrospectively reviewed for clinical and laboratory characteristics in patients with SLE. Disease activity in SLE patients was assessed by the SLE Disease Activity Index (SLEDAI) score. Results: In patients with SLE, serum sFasL levels (383.1±208.9pg/ml) were significantly higher (p<0.001) than those of healthy controls (192.0±84.7pg/ml). sFasL levels in patients with RA (150.8±30.7pg/ml, p=0.014), SSc (115.4±13.5pg/ml, p<0.001), and AOSD (137.5±12.9pg/ml, p=0.001) were significantly lower compared with healthy controls. The frequencies of positive FasL-Fas complex and FasL-IgG complex were higher in patients with SLE (56.8%, 56.8% respectively) than in healthy controls (2.5%, 0% respectively) (p<0.001). All patients with RA or AOSD were negative for FasL-Fas complex and FasL-IgG complex. No patients with SSc were positive for FasL-Fas complex. On the other hand, the positive frequency of FasL-IgG complex was greater in patients with SSc (16.7%) than in healthy controls (0%) (p=0.012). Serum levels of FasL-IgG complexes in active SLE patients (OD 0.467±0.050) were tended to be lower than those in inactive SLE patients (OD 0.509±0.055) (p=0.060). SLEDAI score was tended to be negatively correlated with the serum levels of FasL-IgG complex in patients with SLE (r=-0.308, p=0.068). Conclusion: These results suggest that FasL may possibly play a role in the pathogenesis of SLE.
거리 측정법을 통한 유방 초음파 영상의 컴퓨터 보조 진단(Computer-aided Diagnosis) 시스템
김민정(Min-jeong Kim),최다혜(Da-hye Choi),이승민(Seung-min Lee),민소연(So-yeon Min),윤찬란(Chan-ran Youn),김가연(Ga-yeon Kim),권윤서(Yun-seo Kweon),조현종(Hyun-chong Cho) 대한전자공학회 2016 대한전자공학회 학술대회 Vol.2016 No.11
The Computer-aided Diagnosis System development to diagnose breast cancer can help for radiologists. After extract morphological and texture features of breast masses, we estimate characterization of query mass by applying similarity measures. Then we analysis and compare performance of similarity measures through the Receiver Operating Characteristics(ROC) analysis method. We apply the similarity measures such as Euclidean Distance, Tanimoto Distance and Mahalanobis Distance and compare and analyze each performance of similarity measures. As a result, Mahalanobis Distance measure show outstanding performance in ordinally.
Hydroxychloroquine이 T 세포의 Fas Ligand 대사에 미치는 영향
민준기 ( Jun Ki Min ),이희진 ( Hee Jin Lee ),이원선 ( Won Sun Lee ),박상희 ( Sang Hee Park ),민소연 ( So Youn Min ),조미라 ( Mi La Cho ),조철수 ( Chul Soo Cho ),김호연 ( Ho Youn Kim ) 대한류마티스학회 2000 대한류마티스학회지 Vol.7 No.2
Objective: Hydroxychloroquine (HCQ) is a drug that has been used to treat autoimmune disorders such as rheumatoid arthritis arid systemic lupus erythematosus. However, the specific mechanism for its pharmacologic action has been largely unknown. It has been reported that dysregulation of lymphocytic apoptosis mediated by Fas ligand (FasL) and Fas is associated with the development of autoimmune diseases and HCQ induces apoptosis in peripheral blood lymphocytes. These reports suggest that HCQ may exert its pharmacologic effects through the modulation of FasL and Fas. Therefore, we are intended to investigate the effects of HCQ on the regulation of FasL and Fas. Methods: Jurkat cells or peripheral blood mononuclear cells (PBMNC) were treated with varying concentrations of HCQ. Semiquantative reverse transcription-polymerase chain reaction, Western blotting, flow cytometry, and ELISA were used for this study. Results: HCQ at nontoxic concentrations(50~150μM) caused a dose dependent increase of FasL mRNA expression and FasL in cell lysates. HCQ inhibited the release of intracellular 40 kDa FasL by Jurkat cells which were pulse-stimulated with PHA (50㎍/㎖). Jurkat cells activated with PHA increased membrane bound FasL (mFasL) expression (24.5±4.3%), however Jurkat cells pretreated with HCQ(150μM) followed by PHA administration did not further increase mFasL expression (26.8±1.6%). Addition of different concentrations of HCQ to the cultured PBMNC stimulated with PHA for 24 hours showed increase of soluble FasL (sFasL). The levels of sFasL treated with HCQ zero, 50, 150 and 300μM for 24hours were 38.6±3.0, 43.4±5.1, 77.0±3.6(P<0.05) and 72.3±8.lpg/㎖(P<0.05) respectively. However, fas metabolism was not affected by HCQ. Conclusion: These results suggest that HCQ may exhibit its pharmacological effects by upregulation of FasL gene expression and increased production sFasL without any influence on the Fas metabolism of T cells.
베체트병 환자에서 혈중 Interleukin 15 농도 상승
박경수 ( Kyung Su Park ),민소연 ( So Youn Min ),조미라 ( Mi La Cho ),윤종현 ( Chong Hyeon Yoon ),김용주 ( Yong Ju Kim ),박종서 ( Jong Seo Park ),최진정 ( Jin Jung Choi ),김완욱 ( Wan Uk Kim ),홍연식 ( Youn Sik Hong ),민준기 ( Jun 대한류마티스학회 2002 대한류마티스학회지 Vol.9 No.2
Objective: To evaluate clinical significance of interleukin 15 (IL-15) in patients with Behcet`s disease (BD). Methods: Serum samples were obtained from 31 patients with BD and 29 healthy controls. BD patients were divided into active and inactive group according to the presence of clinical manifestations on the day of sampling. Serum levels of IL-15 and IL-8 were measured by sandwich enzyme-linked immunosorbent assay (ELISA). Results: Serum levels of IL-15 and IL-8 were significantly higher in BD patients than in healthy controls (117.2±26.2 pg/ml versus 51.8±15.4 pg/ml, p<0.01, 287.7±100.9 pg/ml versus 138.5±17.2 pg/ml, p<0.01, respectively). There was a significant correlation between serum levels of IL-15 and IL-8 (r(s)=0.653, p<0.01). BD patients with uveitis showed significantly elevated serum IL-15 levels compared with those without it (161.1±68.8 pg/ml versus 96.4±34.8 pg/ml, p<0.05). Serum levels of IL-15 and IL-8 tended to be higher in active group than in inactive group, but didn`t reach statistical significance. Conclusion: Serum level of IL-15 was elevated in patients with BD, especially those with uveitis, but it did not seem to be useful as a marker of disease activity in BD.
콜라겐 유도 관절염에서 콜라겐 항원 특이 $V{\beta}3$+CD4+T 세포의 선택적 증식
이재선,조미라,이정은,민소연,윤종현,김완욱,민준기,박성환,김호연,Lee, Jae-Seon,Cho, Mi-La,Lee, Jung-Eun,Min, So-Youn,Yoon, Chong-Hyeon,Kim, Wan-Uk,Min, Jun-Ki,Park, Sung-Hwan,Kim, Ho-Youn 대한면역학회 2005 Immune Network Vol.5 No.2
Background: Collagen-induced arthritis (CIA) in mice is animal model of autoimmune disease known as rheumatic arthritis in human. We investigated CII-specific CD4+ T cell receptor usage in CIA mice. Methods: In CIA model, draining lymph node (dLN) CD4+ T cells and splenocytes at $3^{rd},\;5^{th},\;8^{th}$ week, we investigated CII-specific T cell proliferation, production of IL-17, IFN-${\gamma}$, TNF-${\alpha}$, IL-4 and IL-10. And we also performed anti-CII IgG Ab measurements in serum level, TCRV ${\beta}$ usage and T cell clonality with RT-PCR-SSCP analysis. Also, we performed proliferative response against CII when CII-specific T cell subset is deleted. Results: CIA mice showed more increase in the serum level of anti-CII IgG than normal mice after induction of arthritis. And the level of anti-CII IgG2a in CIA mice was increased after $3^{rd}$ week after primary immunization, while anti-CII IgG1 was decreased. Draining LN CD4+ T cells have proliferated against CII stimulation at $3^{rd}$ week after $1^{st}$immunization. CD4+T cells derived from dLN of CIA mice produced proinflammatory cytokine IFN-${\gamma}$, IL-17 etc. Draining LN CD4 T cells of CIA presented higher proportion of CD4+V ${\beta}3$+subset compared to those of normal mice at $3^{rd}$ week after $1^{st}$ immunization, and they were increased in proportion by CII stimulation. Draining LN CD4+ T cells without TCRV ${\beta}3+/V{\beta}8.1/8.2+/V{\beta}$10b+cells were not responsive against CII stimulation. But, CII-reactive response of TCRV ${\beta}3-/V{\beta}8.1/8.2-/V{\beta}$10b- T cells was recovered when $V{\beta}3+$ T cells were added in culture. Conclusion: Our results indicate that CD4+$V{\beta}3+$ T cells are selectively expanded in dLN of CIA mice, and their recovery upon CII re-stimulation in vitro, as well as the production Th1-type cytokines, may play pivotal role in CIA pathogenesis.
Elevated Serum Levels of Both TH1 1 and TH2 Cytokines in Patients with Adult Still`s Disease
민준기 ( Jun Ki Min ),조미라 ( Mi Ra Cho ),민소연 ( So Yeon Min ),김선준 ( Sun June Kim ),김완욱 ( Wan Uk Kim ),홍연식 ( Yeon Sik Hong ),박성환 ( Sung Hwan Park ),조철수 ( Chul Soo Cho ),김호연 ( Ho Youn Kim ) 대한내과학회 1999 대한내과학회 추계학술대회 Vol.57 No.-
The Role of Interleukin-12 in Inflammatory Activity of Patients with Rheumatoid Arthritis
김완욱 ( Wan Uk Kim ),민소연 ( So Youn Min ),조미라 ( Mi La Cho ),민준기 ( Jun Ki Min ),홍연식 ( Yeon Sik Hong ),이상헌 ( Sang Heon Lee ),박성환 ( Sung Hwan Park ),조철수 ( Chul Soo Cho ),김호연 ( Ho Youn Kim ) 대한내과학회 1999 대한내과학회 추계학술대회 Vol.57 No.-
김경운,조미라,이상헌,민소연,박미경,박성환,주대명,김호연,Kim, Kyoung-Woon,Cho, Mi-La,Lee, Sang-Heon,Min, So-Youn,Park, Mi Kyung,Park, Sung-Hwan,Jue, Dae-Myung,Kim, Ho-Youn 대한면역학회 2003 Immune Network Vol.3 No.4
Inflammatory mediators has been recognized as an important role in the pathogenesis of rheumatoid arthritis (RA). IL-17 is increasingly recognized as an important regulator of immune and inflammatory responses, including induction of proinflammatory cytokines and osteoclastic bone resorption. Evidence of the expression and proinflammatory activity of IL-17 has been demonstrated in RA synovium and in animal models of RA. However, the signaling pathways that regulate IL-17 production remain unknown. In the present study, we investigated the role of the phosphatidylinositol 3 kinase (PI3K)-Akt pathway in the regulation of IL-17 production in RA. PBMC were separated from RA (n=24) patients, and stimulated with various agents (anti CD3, anti CD28, PHA, ConA, IL-15). IL-17 levels were determined by sandwich ELISA and RT-PCR. The production of IL-17 was significantly increased in cells treated with anti-CD3 antibody, PHA, IL-15 or MCP-1 (P<0.05). ConA also strongly induced IL-17 production (P<0.001), whereas TNF-alpha, IL-1beta, IL-18 or TGF-beta did not. IL-17 was detected in the PBMC of patients with osteoarthritis (OA) but their expression levels were much lower than those of RA PBMC. Anti-CD3 antibody activated the PI3K-Akt pathway and activation of the PI3K-Akt pathway resulted in a pronounced augmentation of nuclear factor kappaB ($NF-{\kappa}B$). IL-17 production by activated PBMC in RA is completely or partially blocked in the presence of $NF-{\kappa}B$ inhibitor PDTC and PI3K-Akt inhibitor, wortmannin and LY294002, respectively. Whereas the inhibition of AP-1 and extracellular signal-regulated kinase (ERK)1/2 did not affect IL-17 production. These results provide new insight into that PI3K/Akt and $NF-{\kappa}B$ dependent signal transduction pathway could be involved in the overproduction of key inflammatory cytokine, IL-17 in rheumatoid arthritis.