系统性红斑狼疮患者血清γ干扰素诱导的T细胞α趋化因子检测

中华皮肤科杂志 ›› 2003, Vol. 36 ›› Issue (1): 4-6.

系统性红斑狼疮患者血清γ干扰素诱导的T细胞α趋化因子检测

刘伦飞¹, 郑敏¹, 王建有¹, 叶志健²

1. 浙江大学医学院附属第二医院皮肤科, 杭州310009;
2. 龙泉市人民医院皮肤科

收稿日期:2002-01-25 出版日期:2003-01-15 发布日期:2003-01-15
基金资助:
浙江省自然科学基金资助课题(399126)

Serum Level of Interferon-inducible T Cell Alpha Chemoattractant(I-TAC)in Patients With Systemic Lupus Erythematosus

LIU Lun-fei¹, ZHENG Min¹, WANG Jian-you¹, YE Zhi-jian²

Department of Dermatology, The Second Affiliated Hospital, Medical School of Zhejiang University, Hangzhou 310009, China

Received:2002-01-25 Online:2003-01-15 Published:2003-01-15

摘要/Abstract

摘要： 目的探讨血清γ干扰素诱导的T细胞α(I-TAC)趋化因子水平与系统性红斑狼疮(SLE)疾病活动的关系及意义。方法采用双抗体夹心ELISA法检测血清I-TAC水平。结果 ①SLE患者血清I-TAC水平(20.20±6.62ng/mL)明显高于正常人对照(3.13±0.70ng/mL),活动期患者(43.96±14.08ng/mL)高于非活动期患者(2.03±0.46ng/mL);患者血清I-TAC水平与疾病活动指数(r=0.54,t=4.87,P<0.001)、血沉(r=0.47,t=3.80,P<0.001)及ANA对数值(r=0.37,t=3.05,P=0.003)呈正相关,它与补体C3(r=-0.26,t=2.03,P<0.05)呈负相关。②肾损组患者(50.22±16.86ng/mL)血清I-TAC水平明显高于非肾损组患者(7.33±5.11ng/mL)。结论 I-TAC可能参与SLE的发病机制,血清I-TAC水平可作为监测疾病活动程度和肾脏损害的一个指标。

关键词: 红斑狼疮,系统性, 趋化细胞因子类,CXC

Abstract: Objective To determine the relationship between serum interferon-inducible T cell alpha chemoattractant(I-TAC)levels and disease activity in patients with systemic lupus erythematosus(SLE).Methods Serum level of I-TAC was measured by sandwich ELISA.Results ①Serum level of I-TAC was significantly increased in patients with SLE as compared with controls,and significantly higher in patients with active SLE than those of the inactive.Serum level of I-TAC showed significant positive correlation with disease activity,erythrocyte sedimetation rate(ESR),logarithm of serum ANA titer,and negative correlation with serum C3 levels.②Serum level of I-TAC was significantly higher in patients with renal involvement than those without renal diseases.Conclusions These results suggest that I-TAC might be involved in the pathogenesis of SLE,and its serum level might be used as a good indicator for the disease activity of SLE and renal involvement.

Key words: Lupus erythematosus,systemic, Chemokines,CXC

刘伦飞, 郑敏, 王建有, 叶志健. 系统性红斑狼疮患者血清γ干扰素诱导的T细胞α趋化因子检测[J]. 中华皮肤科杂志, 2003, 36(1): 4-6.

LIU Lun-fei, ZHENG Min, WANG Jian-you, YE Zhi-jian. Serum Level of Interferon-inducible T Cell Alpha Chemoattractant(I-TAC)in Patients With Systemic Lupus Erythematosus[J]. Chinese Journal of Dermatology, 2003, 36(1): 4-6.

参考文献

[1] 刘伦飞,郑敏.CXCR3及其配体与皮肤病.国外医学皮肤性病分册,2002,28:166-168.
[2] Becker H, Schauer U, Helmke K.B lymphocyte activation by insoluble anti-μ antibodies in patients with systemic lupus erythematosus. Clin Exp Immunol, 1986,66:365-372.
[3] Bombardier C, Gladman DD, Urowitz MB,et al.Derivation of the SLEDAI. A disease activity index for lupus patients. The Committee on Prognosis Studies in SLE. Arthritis Rheum, 1992,35:630-640.
[4] 郑敏,朱铁城.SLE患者B淋巴细胞增殖功能测定及其临床意义.中华皮肤科杂志,1990,23:90-92.
[5] Arenberg DA, Kunkel SL, Polverini PJ, et al. Interferon-gamma-inducible protein 10 (IP-10) is an angiostatic factor that inhibits human non-small cell lung cancer (NSCLC) tumorigenesis and spontaneous metastases. J Exp Med, 1996,184:981-992.
[6] Khalil M, Inaba K, Steinman R, et al. T cell studies in a peptideinduced model of systemic lupus erythematosus. J Immunol, 2001,166:1667-1674.
[7] Csiszar A, Nagy G, Gergely P, et al. Increased interferon-gamma(IFN-gamma), IL-10 and decreased IL-4 mRNA expression in peripheral blood mononuclear cells (PBMC) from patients with systemic lupus erythematosus (SLE). Clin Exp Immunol, 2000,122:464-470.
[8] Campbell JD, Stinson MJ, Simons FE, et al. In vivo stability of human chemokine and chemokine receptor expression.Hum Immunol,2001,62:668-678.
[9] Alexopoulos E, Seron D, Hartley RB, et al. Lupus nephritis: correlation of interstitial cells with glomerular function. Kidney Int, 1990,37:100-109.
[10] Akahoshi M, Nakashima H, Tanaka Y,et al.Th1/Th2 balance of peripheral T helper cells in systemic lupus erythematosus. Arthritis Rheum, 1999,42:1644-1648.
[11] Masutani K, Akahoshi M, Tsuruya K, et al. Predominance of Th1 immune response in diffuse proliferative lupus nephritis. Arthritis Rheum, 2001,44:2097-2106.
[12] Romagnani P, Beltrame C, Annunziato F, et al. Role for interactions between IP-10/Mig and CXCR3 in proliferative glomerulonephritis.J Am Soc Nephrol, 1999,10:2518-2526.