title: Soluble cytokine receptors in renal vasculitis and lupus nephritis.
abstract: BACKGROUND
  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.
  
  
  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 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: 1st Department of Medicine, 1st Medicine Faculty, Charles University, Prague, Czech Republic. tesarv@beba.cesnet.cz
authors.forename: Vladimír
authors.initials: V
authors.lastname: Tesar
authors.forename: Milan
authors.initials: M
authors.lastname: Jirsa
authors.forename: Tomás
authors.initials: T
authors.lastname: Zima
authors.forename: Marta
authors.initials: M
authors.lastname: Kalousová
authors.forename: Jirina
authors.initials: J
authors.lastname: Bartunková
authors.forename: Alena
authors.initials: A
authors.lastname: Stejskalová
authors.forename: Ctibor
authors.initials: C
authors.lastname: Dostál
authors.forename: Jiri
authors.initials: J
authors.lastname: Zabka
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000097:blood*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D015850:Interleukin-6 / Q000097:blood*; D007674:Kidney Diseases / Q000378:metabolism*; D008181:Lupus Nephritis / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D018121:Receptors, Cytokine / Q000096:biosynthesis*; D019947:Receptors, Interleukin-6 / Q000097:blood*; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood*; D047889:Receptors, Tumor Necrosis Factor, Type II; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis*; D014657:Vasculitis / Q000378:metabolism*
chemical_list: D015703:Antigens, CD; D015850:Interleukin-6; D018121:Receptors, Cytokine; D019947:Receptors, Interleukin-6; D018124:Receptors, Tumor Necrosis Factor; D047889:Receptors, Tumor Necrosis Factor, Type II; D014409:Tumor Necrosis Factor-alpha