CAJ | 학술논문

目的探讨CD3+CD56+淋巴细胞与慢性乙型肝炎(CHB)患者病情变化和转归的关系.方法 CHB患者53例,HBV携带者17例,19名健康体检者为对照组.研究对象均抽取外周血2～3ml,采用流式细胞技术测定CD3+CD56+淋巴细胞,并进一步分析CD3+CD56+淋巴细胞表面CD4,CD8、T细胞抗原受体(TCR)V α 24,TCR α/β以及TCR γ/δ的表达.结果CHB组CD3+CD56+淋巴细胞为7.4%±4.6%,慢性HBV携带者组为4.5%±3.5%,对照组为4.4%±3.7%,CHB组CD3+CD56+淋巴细胞明显升高.3组人群CD3+CD56+淋巴细胞TCR V α 24的表达,差异无统计学意义.慢性HBV携带者组CD3 CD56+细胞表达的TCR V α 24为2.8%±1.4%,明显高于对照组1.7%±1.0%.CHB组CD3+CD56+细胞CD8和TCRα/β的表达分别为61.9%±16.8%和68.1%±16.9%,对照组为49.2%±15.6%和56.4%±17.9%,CHB组均明显高于对照组.CHB组和HBV携带者组TCR γ/δ的表达,分别为29.6%±15.4%和30.5%±14.8%,CHB组和HBV携带者明显低于对照组41.4%±19.4%.CHB重度患者CD3+CD56 1细胞CD8和TCR α/β的表达分别为69.0%±14.0%和76.1%±12.9%,CHB中度患者CD8的表达为66.4%±14.9%,均明显高于CHB轻度患者51.4%±16.2%和62.1%±14.6%. 结论慢性乙型肝炎的活动可能与CD3+CD56+淋巴细胞的CD8高表达有关.
목적 탐토CD3+CD56+림파세포여만성을형간염(CHB)환자병정변화화전귀적관계.방법 CHB환자53례,HBV휴대자17례,19명건강체검자위대조조.연구대상균추취외주혈2～3ml,채용류식세포기술측정CD3+CD56+림파세포,병진일보분석CD3+CD56+림파세포표면CD4,CD8、T세포항원수체(TCR)V α 24,TCR α/β이급TCR γ/δ적표체.결과CHB조CD3+CD56+림파세포위7.4%±4.6%,만성HBV휴대자조위4.5%±3.5%,대조조위4.4%±3.7%,CHB조CD3+CD56+림파세포명현승고.3조인군CD3+CD56+림파세포TCR V α 24적표체,차이무통계학의의.만성HBV휴대자조CD3 CD56+세포표체적TCR V α 24위2.8%±1.4%,명현고우대조조1.7%±1.0%.CHB조CD3+CD56+세포CD8화TCRα/β적표체분별위61.9%±16.8%화68.1%±16.9%,대조조위49.2%±15.6%화56.4%±17.9%,CHB조균명현고우대조조.CHB조화HBV휴대자조TCR γ/δ적표체,분별위29.6%±15.4%화30.5%±14.8%,CHB조화HBV휴대자명현저우대조조41.4%±19.4%.CHB중도환자CD3+CD56 1세포CD8화TCR α/β적표체분별위69.0%±14.0%화76.1%±12.9%,CHB중도환자CD8적표체위66.4%±14.9%,균명현고우CHB경도환자51.4%±16.2%화62.1%±14.6%. 결론 만성을형간염적활동가능여CD3+CD56+림파세포적CD8고표체유관.
Objectives To investigate CD3+CD56+ lymphocytes and their subsets in the peripheral blood of chronic hepatitis B patients and to explore the relationship between these cells and the path,genesis of their diseases. Methods Blood samples from 53 chronic hepatitis B patients, 17 from HBV asymptomatic carriers (ASC) and 19 from healthy controls (HC) were collected, CD3+CD56+ lymphocytes were detected by flow cytometry (FCM), then the CD3+CD56+ lymphocytes were gathered to analyze their expressions of CD4,CD8, TCR V α 24, TCR α/β and TCR γ/δ. Results The number of CD3+CD56+ lymphocytes of chronic hepatitis B patients (7.4±4.6%) was more than those of ASC (4.5% ± 3.5%) and healthy controls (4.4% ±3.7%). The expressions of TCR V α24 on CD3+CD56+ lymphocytes showed no significant differences among the three groups, but the expression ofTCR V α 24 on CD3-CD56+ lymphocytes of ASC (2.8% ± 1.4%)was much more than that of the HC (1.7% ± 1.0%). For the subsets analysis, the CD8 and TCR α/β subsets of CD3+CD56+ lymphocytes of chronic hepatitis B (61.9% ± 16.8% and 68.1% ±16.9%) were significantly higher than those of the HC (49.2% ± 15.6% and 56.4% ± 17.9%), while the TCR γ/δsubsets of chronic hepatitis B and ASC (29.6% ± 15.4% and 30.5% ± 14.8%) were decreased significantly than those of the HC (41.4% ± 19.4%). On the other hand, the CD8 and TCR α/β subsets of CD3+CD56+ lymphocytes of severe chronic hepatitis B (69.0% ± 14.0% and 76.1% ±12.9%) and CD8 subsets of moderate chronic hepatitis B patients (66.4% ± 14.9%) were significantly higher than those of the mild chronic hepatitis B patients (51.4% ± 16.2% and 62.1% ± 14.6%). Conclusion The pathogenesis of chronic hepatitis B may positively relate to the high expression of CD8 on the CD3+CD56+ lymphocytes.