09 January 2002
Med Sci Monit 2002; 8(1): BR24-29 :: ID: 420974
BACKGROUND: The activation of various cytokines, e.g. TNFalpha, IL-1 and/orIL-6, may play an important role in the pathogenesis of renal vasculitis and lupus nephritis (LN). Thesystemic effect of these cytokines may be modulated by their circulating soluble receptors. The plasmalevels 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. RESULTS:Patients with LN had increased plasma levels of TNFalpha, sTNF-RII, IL-6 and sIL-6R in comparison withcontrols. Patients with ANCA-A also had increased plasma levels of TNFalpha, sTNF-RII and sIL-6R in comparisonwith controls, but the increase in the plasma level of IL-6 was not statistically significant, due tothe large standard deviation. Patients with ANCA-R had increased plasma levels of sTNF-RII in comparisonto controls, but the plasma levels of TNFalpha were significantly lower in ANCA-R than in ANCA-A. Whilethe 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. CONCLUSIONS:While increased plasma levels of TNFalpha may be a nonspecific marker of the activity of ANCA-positiverenal vasculitis and LN, plasma levels of sTNF-RII are also increased in patients with ANCA-positiverenal vasculitis in remission. Increased plasma levels of sTNF-RII may inhibit the systemic effects ofTNFalpha, but may also prolong the half-life of its active form. Plasma levels of sIL-6R are increasedboth in ANCA-A and in LN, but their increase is much less pronounced than that of sTNF-RII and cannoteffectively block the systemic effects of IL-6.
Keywords: Antigens, CD, Enzyme-Linked Immunosorbent Assay, Interleukin-6, Kidney Diseases, lupus nephritis, Receptors, Cytokine, Receptors, Interleukin-6, Receptors, Tumor Necrosis Factor, Receptors, Tumor Necrosis Factor, Type II, Research Support, Non-U.S. Gov, Vasculitis
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