中华风湿病学杂志
中華風濕病學雜誌
중화풍습병학잡지
CHINESE JOURNAL OF RHEUMATOLOGY
2008年
10期
660-662
,共3页
庞莉萍%王丽莎%郝慧琴%索塔林%方显峰%贾俊英%黄烽%唐捷
龐莉萍%王麗莎%郝慧琴%索塔林%方顯峰%賈俊英%黃烽%唐捷
방리평%왕려사%학혜금%색탑림%방현봉%가준영%황봉%당첩
脊柱炎,强直性%依那西普%T淋巴细胞%免疫酶技术%肿瘤坏死因子α
脊柱炎,彊直性%依那西普%T淋巴細胞%免疫酶技術%腫瘤壞死因子α
척주염,강직성%의나서보%T림파세포%면역매기술%종류배사인자α
Spondylitis,ankylosing%Etanereept%T-lymphocytes%Immunoenzyme technique%Tu-mor necrosis factor αlpha
目的 研究肿瘤坏死因子(TNF)-α抑制剂依那西普(Etanercepl)对强直性脊柱炎(AS)患者外周血T细胞活性的影响.方法 10例健康志愿者,40例活动性AS患者,随机给予依那西普(50 mg,皮下注射,每周1次)或安慰剂治疗,治疗前后分离外周血单个核细胞(PBMC),酶联免疫斑点法(ELISPOT)分别检测分泌TNF-α、白细胞介素(IL)-2、干扰素(IFN)-γ的细胞数量.WST-1法检测T细胞增殖.结果 依那西普治疗后,分泌TNF-α的单核细胞数量减少;抗CD3和抗CD28抗体刺激后,分泌IL-2和IFN-γ的T细胞数量减少.CD4+/CD8+T细胞增殖没有明显变化.结论 抗TNF-α的治疗降低了AS患者外周血T细胞的活性,改善了AS患者病情.
目的 研究腫瘤壞死因子(TNF)-α抑製劑依那西普(Etanercepl)對彊直性脊柱炎(AS)患者外週血T細胞活性的影響.方法 10例健康誌願者,40例活動性AS患者,隨機給予依那西普(50 mg,皮下註射,每週1次)或安慰劑治療,治療前後分離外週血單箇覈細胞(PBMC),酶聯免疫斑點法(ELISPOT)分彆檢測分泌TNF-α、白細胞介素(IL)-2、榦擾素(IFN)-γ的細胞數量.WST-1法檢測T細胞增殖.結果 依那西普治療後,分泌TNF-α的單覈細胞數量減少;抗CD3和抗CD28抗體刺激後,分泌IL-2和IFN-γ的T細胞數量減少.CD4+/CD8+T細胞增殖沒有明顯變化.結論 抗TNF-α的治療降低瞭AS患者外週血T細胞的活性,改善瞭AS患者病情.
목적 연구종류배사인자(TNF)-α억제제의나서보(Etanercepl)대강직성척주염(AS)환자외주혈T세포활성적영향.방법 10례건강지원자,40례활동성AS환자,수궤급여의나서보(50 mg,피하주사,매주1차)혹안위제치료,치료전후분리외주혈단개핵세포(PBMC),매련면역반점법(ELISPOT)분별검측분비TNF-α、백세포개소(IL)-2、간우소(IFN)-γ적세포수량.WST-1법검측T세포증식.결과 의나서보치료후,분비TNF-α적단핵세포수량감소;항CD3화항CD28항체자격후,분비IL-2화IFN-γ적T세포수량감소.CD4+/CD8+T세포증식몰유명현변화.결론 항TNF-α적치료강저료AS환자외주혈T세포적활성,개선료AS환자병정.
Objective To study the effect of TNF-α antagonist (etanercept) treatment on the peripheral T cell reactivity of ankylosing spondylitis (AS) patients. Methods Peripheral blood mononuclear cells (PBMC) were collected from 40 patients with AS at baseline, after two and six weeks of etanercept treatment or placebo and from healthy controls. The number of cells that secret TNF-α,IL-2 and IFN-γwas respectively detected by ELISPOT. CD+/CD8+ T cell proliferation was assayed with WST-1 live cell staining method. Results After 2 and 6 weeks of etanercept treatment, the number of TNF-α secreting monocytes was decreased. Although the T cell proliferation rate was not reduced, the number of T cells secreting IL-2 and IFN-γ under anti-CD3/anti-CD28 stimulation was significantly decreased. Conclusion The anti-TNF-α therapy suppresses the functions of effector T cells. The reduced T cell reactivity may contribute to the efficacy of the TNF-α antagonist therapy in AS patients.