Tesar Vladimír, Jirsa Milan, Zima Tomás, Kalousová Marta, Bartunková Jirina, Stejskalová Alena, Dostál Ctibor, Zabka Jiri
1st Department of Medicine, 1st Medicine Faculty, Charles University, Prague, Czech Republic.
Med Sci Monit. 2002 Jan;8(1):BR24-9.
The activation of various cytokines, e.g. TNFalpha, IL-1 and/or IL-6, may play an important role in the pathogenesis of renal vasculitis and lupus nephritis (LN). The systemic effect of these cytokines may be modulated by their circulating soluble receptors. The plasma levels of cytokine receptors may thus also be markers of the activation of these cytokines.
MATERIAL/METHODS: The plasma levels of TNFalpha, its soluble receptor p75 (sTNF-RII), IL-6, and the soluble IL-6 receptor (sIL-6R) were measured using ELISA in 17 patients with ANCA-positive renal vasculitis (12 active - ANCA-A, 7 in remission ANCA-R), 9 patients with active lupus nephritis (LN), and 5 healthy subjects.
Patients with LN had increased plasma levels of TNFalpha, sTNF-RII, IL-6 and sIL-6R in comparison with controls. Patients with ANCA-A also had increased plasma levels of TNFalpha, sTNF-RII and sIL-6R in comparison with controls, but the increase in the plasma level of IL-6 was not statistically significant, due to the large standard deviation. Patients with ANCA-R had increased plasma levels of sTNF-RII in comparison to controls, but the plasma levels of TNFalpha were significantly lower in ANCA-R than in ANCA-A. While the ratio of TNFalpha to sTNF-RII was significantly lower in all groups of patients than in the controls, the ratio of IL-6 to sIL-6R was significantly increased only in LN in comparison to controls.
While increased plasma levels of TNFalpha may be a nonspecific marker of the activity of ANCA-positive renal vasculitis and LN, plasma levels of sTNF-RII are also increased in patients with ANCA-positive renal vasculitis in remission. Increased plasma levels of sTNF-RII may inhibit the systemic effects of TNFalpha, but may also prolong the half-life of its active form. Plasma levels of sIL-6R are increased both in ANCA-A and in LN, but their increase is much less pronounced than that of sTNF-RII and cannot effectively block the systemic effects of IL-6.
多种细胞因子如肿瘤坏死因子α(TNFα)、白细胞介素-1(IL-1)和/或白细胞介素-6(IL-6)的激活可能在肾血管炎和狼疮性肾炎(LN)的发病机制中起重要作用。这些细胞因子的全身效应可能受其循环可溶性受体的调节。因此,细胞因子受体的血浆水平也可能是这些细胞因子激活的标志物。
材料/方法:采用酶联免疫吸附测定法(ELISA)检测17例抗中性粒细胞胞浆抗体(ANCA)阳性肾血管炎患者(12例活动期 - ANCA-A,7例缓解期ANCA-R)、9例活动期狼疮性肾炎(LN)患者和5例健康受试者血浆中TNFα、其可溶性受体p75(sTNF-RII)、IL-6及可溶性IL-6受体(sIL-6R)的水平。
与对照组相比,LN患者血浆中TNFα、sTNF-RII、IL-6和sIL-6R水平升高。与对照组相比,ANCA-A患者血浆中TNFα、sTNF-RII和sIL-6R水平也升高,但由于标准差较大,IL-6血浆水平的升高无统计学意义。与对照组相比,ANCA-R患者血浆中sTNF-RII水平升高,但ANCA-R患者血浆中TNFα水平显著低于ANCA-A患者。虽然所有患者组中TNFα与sTNF-RII的比值均显著低于对照组,但与对照组相比,仅LN患者中IL-6与sIL-6R的比值显著升高。
虽然TNFα血浆水平升高可能是ANCA阳性肾血管炎和LN活动的非特异性标志物,但缓解期ANCA阳性肾血管炎患者血浆中sTNF-RII水平也升高。sTNF-RII血浆水平升高可能抑制TNFα的全身效应,但也可能延长其活性形式的半衰期。ANCA-A和LN患者血浆中sIL-6R水平均升高,但其升高程度远不如sTNF-RII明显,且不能有效阻断IL-6的全身效应。