中华皮肤科杂志
中華皮膚科雜誌
중화피부과잡지
Chinese Journal of Dermatology
2012年
3期
169-172
,共4页
红斑狼疮,系统性%白细胞介素17%T淋巴细胞,辅助诱导%RORγt
紅斑狼瘡,繫統性%白細胞介素17%T淋巴細胞,輔助誘導%RORγt
홍반랑창,계통성%백세포개소17%T림파세포,보조유도%RORγt
Lupus erythematosus,systemic%Interleukin-17%T-lymphocytes,helper-inducer%RORγt
目的 探讨辅助性T(Th)17细胞介导的炎症损伤与系统性红斑狼疮(SLE)的关系.方法 采用酶联免疫吸附试验(ELISA)检测102例SLE患者及68例健康对照血清白介素17A(IL-17A)水平；实时荧光定量聚合酶链反应方法相对定量分析27例SLE患者及13例健康对照外周血单一核细胞(PBMC)中孤核受体γt(RORγt)基因表达水平；分析血清IL-17A水平与RORγt基因表达之间及其分别与SLE疾病活动度(SLEDAI)、SLE是否合并肾脏病变的关系.结果 102例SLE患者血清IL-17A水平[14.75(5.12 ～ 69.76) ng/L]较68例健康对照组[5.77 (2.22 ～ 9.60) ng/L]显著升高(P＜0.01).102例SLE患者血清IL-17A与血清C反应蛋白、血浆肌酐、尿管型呈正相关(分别为r=0.33、P＜0.01,r=0.26、P＜0.05,r=0.27、P＜ 0.05)；与SLEDAI无显著相关(P＞0.05).27例SLE患者RORγt基因表达水平较13例健康对照组显著升高[1 (0.40 ～ 2.62)和0.19 (0.15～0.75),P＜ 0.01].27例SLE患者RORγt基因表达水平与血清IL-17A水平呈正相关(r=0.47,P＜ 0.01),与血清补体3之间呈负相关(r=-0.46,P＜0.05).SLE病情高活动组与低活动组、SLE合并肾脏病变与SLE无合并肾脏病变组间血清IL-17A、RORγt基因表达水平差异均无统计学意义(P值均＞ 0.05).结论 Th17细胞介导的炎症损伤可能参与了SLE的发病,与SLE肾脏病变可能有关,但其可能不是SLE病情活动惟一的影响因素,在SLE及SLE肾脏受累中可能均不是主导因素.
目的 探討輔助性T(Th)17細胞介導的炎癥損傷與繫統性紅斑狼瘡(SLE)的關繫.方法 採用酶聯免疫吸附試驗(ELISA)檢測102例SLE患者及68例健康對照血清白介素17A(IL-17A)水平；實時熒光定量聚閤酶鏈反應方法相對定量分析27例SLE患者及13例健康對照外週血單一覈細胞(PBMC)中孤覈受體γt(RORγt)基因錶達水平；分析血清IL-17A水平與RORγt基因錶達之間及其分彆與SLE疾病活動度(SLEDAI)、SLE是否閤併腎髒病變的關繫.結果 102例SLE患者血清IL-17A水平[14.75(5.12 ～ 69.76) ng/L]較68例健康對照組[5.77 (2.22 ～ 9.60) ng/L]顯著升高(P＜0.01).102例SLE患者血清IL-17A與血清C反應蛋白、血漿肌酐、尿管型呈正相關(分彆為r=0.33、P＜0.01,r=0.26、P＜0.05,r=0.27、P＜ 0.05)；與SLEDAI無顯著相關(P＞0.05).27例SLE患者RORγt基因錶達水平較13例健康對照組顯著升高[1 (0.40 ～ 2.62)和0.19 (0.15～0.75),P＜ 0.01].27例SLE患者RORγt基因錶達水平與血清IL-17A水平呈正相關(r=0.47,P＜ 0.01),與血清補體3之間呈負相關(r=-0.46,P＜0.05).SLE病情高活動組與低活動組、SLE閤併腎髒病變與SLE無閤併腎髒病變組間血清IL-17A、RORγt基因錶達水平差異均無統計學意義(P值均＞ 0.05).結論 Th17細胞介導的炎癥損傷可能參與瞭SLE的髮病,與SLE腎髒病變可能有關,但其可能不是SLE病情活動惟一的影響因素,在SLE及SLE腎髒受纍中可能均不是主導因素.
목적 탐토보조성T(Th)17세포개도적염증손상여계통성홍반랑창(SLE)적관계.방법 채용매련면역흡부시험(ELISA)검측102례SLE환자급68례건강대조혈청백개소17A(IL-17A)수평；실시형광정량취합매련반응방법상대정량분석27례SLE환자급13례건강대조외주혈단일핵세포(PBMC)중고핵수체γt(RORγt)기인표체수평；분석혈청IL-17A수평여RORγt기인표체지간급기분별여SLE질병활동도(SLEDAI)、SLE시부합병신장병변적관계.결과 102례SLE환자혈청IL-17A수평[14.75(5.12 ～ 69.76) ng/L]교68례건강대조조[5.77 (2.22 ～ 9.60) ng/L]현저승고(P＜0.01).102례SLE환자혈청IL-17A여혈청C반응단백、혈장기항、뇨관형정정상관(분별위r=0.33、P＜0.01,r=0.26、P＜0.05,r=0.27、P＜ 0.05)；여SLEDAI무현저상관(P＞0.05).27례SLE환자RORγt기인표체수평교13례건강대조조현저승고[1 (0.40 ～ 2.62)화0.19 (0.15～0.75),P＜ 0.01].27례SLE환자RORγt기인표체수평여혈청IL-17A수평정정상관(r=0.47,P＜ 0.01),여혈청보체3지간정부상관(r=-0.46,P＜0.05).SLE병정고활동조여저활동조、SLE합병신장병변여SLE무합병신장병변조간혈청IL-17A、RORγt기인표체수평차이균무통계학의의(P치균＞ 0.05).결론 Th17세포개도적염증손상가능삼여료SLE적발병,여SLE신장병변가능유관,단기가능불시SLE병정활동유일적영향인소,재SLE급SLE신장수루중가능균불시주도인소.
Objective To estimate the relationship between T helper 17 (Th17) cell-mediated inflammatory damage and systemic lupus erythematosus (SLE).Methods Serum interleukin (IL)-17A levels were measured by enzyme-linked immunosorbent assay (ELISA) in 102 patients with SLE and 68 normal human controls.Real time-quantitative PCR was used to quantify the expression levels of RORγt mRNA in peripheral blood mononuclear cells (PBMCs) from 27 patients with SLE and 13 normal human controls.Linear regression analysis and Spearman correlation analysis were conducted to assess the relationship of serum IL-17A levels with RORγt mRNA expression,SLE disease activity index (SLEDAI),and the concurrence of renal damage.Results There was a significant increase in serum IL-17A levels and RORγt mRNA expression in patients with SLE compared with the normal controls [ 14.75 (5.12 - 69.76) vs.5.77 (2.22 - 9.60) ng/L,P ＜ 0.01; 1 (0.40 - 2.62)vs.0.19 (0.15 - 0.75 ),P ＜ 0.01 ].The serum levels of IL-17A in patients with SLE were positively correlated with the levels of serum C-reactive protein,plasma creatinine and prevalence of urinary cast (r =0.33,P ＜ 0.01; r =0.26,P ＜ 0.05; r =0.27,P ＜ 0.05),but unrelated to SLEDAI (P ＞ 0.05).The mRNA expression level of RORγt was positively correlated with serum IL-17A levels (r =0.47,P ＜ 0.01),but negatively correlated with serum C3 levels in patients with SLE(r =-0.46,P ＜ 0.05).There was no significant difference in the levels of serum IL-17A or RORγt mRNA expression between patients with highly and lowly active SLE or between patients with and without renal damage (all P ＞ 0.05).Conclusions Th17 cell-mediated inflammatory damage may be involved in the pathogenesis of SLE,and associated with renal damage,but is unlikely the only factor affecting the activity of SLE or predominant factor in the pathogenesis of SLE and concurrent renal damage.
