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활동성 전신홍반루푸스 환자의 FSChigh Memory B 세포의 특징 분석
전주연 ( Joo Yeon Jhun ),김영주 ( Young Joo Kim ),주지현 ( Ji Hyun Ju ),박성환 ( Sung Hwan Park ),장숙희 ( Soog Hee Chang ),김호연 ( Ho Youn Kim ) 대한류마티스학회 2007 대한류마티스학회지 Vol.14 No.3
Objective: To determine phenotypic and functional characteristics of memory B cells in patients with systemic lupus erythematosus (SLE). Methods: The percentage of memory B cell subsets in peripheral blood mononuclear cells (PBMC) from normal control (n=11), inactive (n=15) and active (n=10) SLE patients was determined by Fluorescence Activated Cell Sorter (FACS). In addition, the activation status of memory B cells was measured by the surface expression of CD86 (B7-2). The production of antibodies to chromatin and dsDNA (IgG and IgM type) by isolated memory B cell subsets was examined by enzyme-linked immunosorbent assay (ELISA). Results: In this study, we analyzed 2 subtypes of memory B cells: FSC (Forward Side Scatter)low and FSChigh memory B cell. The percentage of both subtypes from active and inactive SLE patients was significantly reduced compared to that of normal controls (p<0.01). In addition, the expression of activation markers, CD86 on FSChigh memory B cells from active SLE patients was higher than those of inactive SLE patients and normal controls (p=0.014). Upon stimulation with CpG and IL-15 in vitro for 8 days, isolated FSChigh memory B cells from active SLE patients revealed augmented production of autoantibodies to chromatin and dsDNA. Conclusion: Our results suggest that abnormally activated FSChigh memory B cells from active SLE patients might be involved in spontaneous production of autoantibodies and induce transition from inactive to active phase of the patients.
( Hee Yeon Kim ),( Jong Young Choi ),( Chang Wook Kim ),( Chang Don Lee ),( Seung Kew Yoon ),( Si Hyun Bae ),( Nam Ik Han ),( Joo Yeon Jhun ),( Mi La Cho ),( Yang Mi Heo ) 대한간학회 2013 춘·추계 학술대회 (KASL) Vol.2013 No.1
Background: High-mobility group box 1 (HMGB1), a ligand for receptor for advanced glycation end products (RAGE), is released from necrotic hepatocytes, and contribute to the pathogenesis of chronic hepatitis. T helper 17 cells (Th17) also have been suggested to participate in the pathogenesis of chronic hepatitis B (CHB) infection. We investigated the role of HMGB1-RAGE-Th17 axis in the pathogenesis of CHB. Methods: The levels of HMGB1 and IL-17 expression were detected by Western blotting and real-time RT-PCR in patients with CHB. The effect of HMGB1-RAGE on the immune activity of Th17 cells and vice versa, was assessed by an induction assay. The levels of IL-17 expression was determined by RT-PCR and Western blotting after blocking RAGE. Results: The levels of HMGB1 and IL-17 expression were higher in CHB patients than in controls. The levels of IL-17 were significantly elevated when PBMCs were stimulated with HMGB1 in vitro, and vice versa. The levels of IL-17 expression was significantly reduced when PBMCs were treated with competitors for RAGE in vitro. Conclusions: HMGB1-RAGE induces the generation of IL- 17, which mediates the pathogenesis of CHB infection. It is suggested that HMGB1 might be a potential target for controlling hepatitis B infection by suppressing Th17 activity.
Kim, Hee Yeon,Jhun, Joo Yeon,Cho, Mi-La,Choi, Jong Young,Byun, Jae Kyeong,Kim, Eun-Kyung,Yoon, Seung Kew,Bae, Si Hyun,Chung, Byung Ha,Yang, Chul Woo Springer International 2014 Journal of gastroenterology Vol.49 No.8
<P>Interleukin (IL)-17-producing CD4(+) T cells (Th17) have been shown to play crucial roles in the pathogenesis of hepatitis B virus (HBV)-associated acute-on-chronic liver failure (ACLF). However, the mechanism underlying the enhanced Th17 responses in these patients remains elusive. In this study, the relevance of the IL-6/signal transducer and activator of transcription 3 (STAT3)/mammalian target of rapamycin (mTOR)/Th17 loop in HBV-associated ACLF was investigated.</P>
윤보영,조미라,Yeon-Sik Hong,Joo-Yeon Jhun,Mi-Kyung Park,Kyung-Su Park,Sung-Hwan Park,Ho-Youn Kim 대한면역학회 2007 Immune Network Vol.7 No.3
BACKGROUND: Regulatory T cells (Tregs) have been investigated intensively for some decades. These cells regulate the immune system, prevent overactivated immune responses and can be used therapeutically. For rheumatoid arthritis (RA), understanding the functions and status of Tregs is an important step for understanding immune regulation in this autoimmune disease.0aMETHODS: We investigated the percentages, phenotypes and suppressive functions of CD4RESULTS: The percentages were higher in the patients (n25oing inflammation ineffectively. It might be possible to apply IL-10 to induce the proliferation of IL-10-producing Tregs as therapy for RA
Myung-Ju Oh(오명주),Joo-Yeon Ha(하주연),Byung H. Jhun(전병학) 한국생명과학회 2022 생명과학회지 Vol.32 No.11
Breast cancer anti-estrogen resistance 3 (BCAR3)는 유방암에서 항에스트로겐 내성을 유도하는 유전자들 중의 하나로 발견되었다. 우리는 이미 BCAR3가 c-jun, activator protein-1, serum response element의 promoter 등을 활성화하는 것을 보고하였다. 본 연구에서 우리는 정상 유방세포인 MCF-12A에서 estrogen response element (ERE) 활성에서의 BCAR3의 기능을 조사하였다. BCAR3의 발현이 ERE를 활성화하는 것을 발견하였다. 이 ERE 활성화는 17β-estradiol에 의해 더욱 증가하였고, 이는 항에스트론겐인 tamoxifen에 의해 억제되지 않았다. 다음으로 우리는 ERE 활성화를 이끄는 BCAR3의 신호전달 경로를 연구하였다. BCAR3에 의한 ERE 활성화는 phosphatidylinositol (PI) 3-kinase 경로 억제제인 LY294002와 AZD5363에 의해서는 억제되었으나, Mitogen-activated protein kinase 경로 억제제인 PD98059와 U0126에 의해서는 억제되지 않았다. ERE 활성화는 PI3-kinase의 catalytic subunit p110α와 Akt의 active mutant에 의해서는 유도되었고, 이 활성화는 추가적인 BCAR3에 의해서는 더욱 증가하지 않았다. 이러한 결과로부터 우리는 BCAR3가 PI3-kinase/Akt 신호전달경로를 통하여 ERE 활성화에 중요한 역할을 하는 것을 제시한다. Breast cancer anti-estrogen resistance 3 (BCAR3) has been identified as one of the genes that induces anti-estrogen resistance in breast cancer. We have previously reported that BCAR3 activates promoters of c-Jun, activator protein-1, and the serum response element. In this study, we investigated the functional role of BCAR3 in the activation of the estrogen response element (ERE) in normal human breast MCF-12A cells. Transient expression of BCAR3 induced ERE activation, which was further increased by 17β-estradiol treatment but was not blocked by the anti-estrogen tamoxifen. Next, we studied the signaling pathway of BCAR3 leading to ERE activation. BCAR3-mediated ERE activation was inhibited by LY294002 and AZD5363, inhibitors of the phosphatidylinositol (PI) 3-kinase pathway, but not by PD98059 and U0126, inhibitors of the mitogen-activated protein kinase pathway. ERE activation was induced by the catalytic subunit p110α of PI3-kinase or the active mutant of Akt, and this activation was not further increased by additional BCAR3 transfection. Based on these results, we propose that BCAR3 plays an important role in ERE activation through the PI3-kinase/Akt pathway in human breast MCF-12A cells.
Kim, Eun Kyung,Lee, Seung Hoon,Jhun, Joo Yeon,Byun, Jae Kyeong,Jeong, Jeong Hee,Lee, Seon-Young,Kim, Jae Kyung,Choi, Jong Young,Cho, Mi-La Hindawi Publishing Corporation 2016 MEDIATORS OF INFLAMMATION Vol.2016 No.-
<P>Obesity and its associated metabolic disorders are related to the onset of fatty liver and the balance of white adipose tissue (WAT) and brown adipose tissue (BAT). We hypothesized that metformin, an effective pharmacological treatment for type 2 diabetes, would inhibit white adipogenesis, fatty liver, and metabolic dysfunction. Metformin was treated daily for 14 weeks in a high-fat dieting C57BL/6J mice. Serum biomarkers were analyzed and protein level was assessed using confocal staining or flow cytometry. The development of lipid drops in the liver cells and white adipocyte was measured using hematoxylin and eosin or Oil Red O stains. Gene expressions were analyzed with quantitative real-time PCR. Metformin treatment decreased the body weight and improved the metabolic profile of obese mice. In obese mice, metformin also induced the expression of BAT-related markers and increased fibroblast growth factor (FGF) 21 expression in the liver and in white adipocyte. Metformin suppressed white adipocyte differentiation via induction of FGF21. Metformin improves Treg/Th17 balance in CD4+ T cells in mice with high-fat diet-induced obesity. Metformin also improves glucose metabolism and metabolic disorder. Interleukin-17 deficiency also decreases inflammation in mice. Therefore, metformin may be therapeutically useful for the treatment of obesity and metabolic dysfunction. </P>
Yoon, Bo-Young,Cho, Mi-La,Hong, Yeon-Sik,Jhun, Joo-Yeon,Park, Mi-Kyung,Park, Kyung-Su,Park, Sung-Hwan,Kim, Ho-Youn 대한면역학회 2007 Immune Network Vol.7 No.3
Regulatory T cells (Tregs) have been investigated intensively for some decades. These cells regulate the immune system, prevent overactivated immune responses and can be used therapeutically. For rheumatoid arthritis (RA), understanding the functions and status of Tregs is an important step for understanding immune regulation in this autoimmune disease. Methods: We investigated the percentages, phenotypes and suppressive functions of CD4<sup>+</sup>CD25<sup>+</sup> Tregs in peripheral blood (PB) of patients with RA. Results: The percentages were higher in the patients (n=12) than in healthy controls (n=10), and the cells expressed the CD45RB<sup>low</sup>, CTLA-4 and CCR7 phenotypes. We also investigated the expression of Foxp3 and secretion of interleukin (IL)-10 induced CD4<sup>+</sup>CD25<sup>+</sup> Tcells by anti-CD3 antibody treatment. A suppressive function of the patients' cells was shown through coculture with CD4<sup>+</sup>CD25^- T cells in vitro. Conclusion: We suggest that, despite their increased numbers and suppressive function, they manage the ongoing inflammation ineffectively. It might be possible to apply IL-10 to induce the proliferation of IL-10-producing Tregs as therapy for RA.