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전신홍반루푸스 환자에서 IFN-α에 의한 CD4+ T 림프구의 ERK Phosphorylation의 감소
류완희 대한류마티스학회 2006 대한류마티스학회지 Vol.13 No.4
Objective: CD4+ T cells from patients with systemic lupus erythematosus (SLE) display aberrant TCR signaling and IFN-α plays critical roles in the pathogenesis of SLE; however, the effects of IFN-α on disease-associated TCR signaling defects remain unknown. This study investigated the ERK phosphorylation during TCR triggering and the effects of IFN-α on ERK signaling in CD4+ T cells. Methods: CD4+ T lymphocytes were sorted from PBMC using magnetic beads in patients with SLE who met the 1982 revised ACR criteria for SLE and age-matched healthy controls. The phosphorylation of ERK 1/2 was analyzed by flow cytometry and mean fluorescent intensity was measured to define the degree of phosphorylation of ERK. In some experiments, anti-CD3 stimulation was performed after preincubation with patient or control serum, diluted in tissue culture media, with or without addition of an anti-IFN-α antibody. The serum level of IFN-α was measured by ELISA. Results: ERK-1/2 phosphorylation was decreased in CD4+ T cells of lupus patients than healthy controls and associated with disease activity. Pre-incubation of control CD4+ T cells with allogeneic lupus plasma decreased ERK-1/2 phosphorylation more than allogeneic control and RA plasma and this was reversed by anti-IFN-α Ab. Accordingly, ERK-1/2 phosphorylation was decreased in control CD4+ T cells pre-incubation with lupus plasma with high IFN-α levels more than lupus plasma with non-detectable IFN-α levels. Recombinant IFN-α inhibited TCR-mediated ERK-1/2 phosphorylation dose-dependently. Conclusion: These results suggest that IFN-α stimulation in vivo may underlie the aberrant TCR-mediated MAPK signaling in lupus CD4+ T cells and associated with disease pathogenesis.
제2형 당뇨병 환자에서 App E 지단백 유전자형 다형성과 혈청 지질과의 관계
류완희,염정필,김용성,윤경하,이규호,박지현,김현각,박태선,백흥선,김달식 의과학연구소 2000 全北醫大論文集 Vol.24 No.2
Background and purpose : Apolipoprotein E (apo E) has important function for lipoprotein metabolism as a low density lipoprotein (LDL) receptor and hepatic apo E receptor. Apo E has three isoforms, E2, E3 and E4. The purpose of this study is to evaluate the serum lipid profile depending on apo E genotype in the type 2 diabetic patients. Materials and Methods : Two hundred thirty four type 2 diabetic patients and ninty four controls were included in this study. The serum lipid profiles were measured and apo E genotypes were determined by modified Amplification Refractory Mutation system (ARMS) and classified into E2, E3 and E4 subgroups. Results : The apo E genotype frequencies in type 2 diabetic patients were as follows; 70.9% for ε3/3, 15.0% for ε3/4, 8.5% for ε3/2, 2.1% for ε2/2, 2.1% for ε4/4, 1.3% for ε2/4. The calculated apo E allele frequencies were 0.069 for ε2, 0.819 for ε3, 0.112 for ε4. There were no significant differences betwwen type 2 diabetic patients and controls in apo E genotype, and allele frequencies. Mean level of the serum HDL-cholesterol was significantly lower in E4 group than E2 and E3. The subjects with apo ε4 allele had sgnificantly lower level of HDL-cholesterol than the subjects without ε4 allele and subjects with apo ε2 were associated with higher level of LDL-cholesterol and of triglyceride in type 2 diabetic patients. Conclusion : Apo E polymorphism plays an important role in dtermining individual differences in serum lipid level in type 2 diabetic patients.