title: Circulating levels of tumor necrosis factor soluble receptors in systemic lupus erythematosus are significantly higher than in other rheumatic diseases and correlate with disease activity.
abstract: OBJECTIVE
  To investigate the difference in acute phase protein responses between patients with systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and spondyloarthropathies (SpA).
  
  
  METHODS
  Circulating levels of cytokines inducing the production of acute phase proteins such as interleukin (IL)-6, IL-1 beta, and tumor necrosis factor (TNF)-alpha, and of cytokine inhibitors such as TNF soluble receptors (TNF-sR55 and TNF-sR75) and IL-1 receptor antagonist (IL-1ra), were measured in 2 cohorts of patients. The first cohort included 52 patients with SLE and 22 with RA, and the second included 21 with SLE, 20 with RA, and 18 with SpA. An examination at the time of blood collection and the Systemic Lupus Activity Measure (SLAM) index were used to assess disease activity in patients with SLE. Serum levels of IL-6 were measured using a biological assay, and concentrations of IL-1 beta, TNF-alpha, TNF-sR55, TNF-sR75, and IL-1ra were assessed by immunoassays.
  
  
  RESULTS
  Although C-reactive protein (CRP) levels were significantly lower in SLE than in RA or SpA, the concentrations of circulating IL-6 or TNF-alpha were higher in SLE. The most striking observation was that TNF-sR levels were significantly higher in SLE than in RA or SpA. The TNF-alpha: TNF-sR ratio was also significantly lower in SLE than in RA. TNF-sR55 and TNF-sR75 levels correlated with disease activity in SLE.
  
  
  CONCLUSIONS
  The weak acute phase protein response in SLE may be explained by a decreased ratio between inducing cytokines and their inhibitors. In addition, TNF-sR may prove a useful biological marker for the followup of SLE, where acute phase protein response is generally low during disease exacerbations.
authors.affiliation: Division of Rheumatology, University Hospital of Geneva, Switzerland.
authors.forename: C
authors.initials: C
authors.lastname: Gabay
authors.forename: N
authors.initials: N
authors.lastname: Cakir
authors.forename: F
authors.initials: F
authors.lastname: Moral
authors.forename: P
authors.initials: P
authors.lastname: Roux-Lombard
authors.forename: O
authors.initials: O
authors.lastname: Meyer
authors.forename: J M
authors.initials: JM
authors.lastname: Dayer
authors.forename: T
authors.initials: T
authors.lastname: Vischer
authors.forename: H
authors.initials: H
authors.lastname: Yazici
authors.forename: P A
authors.initials: PA
authors.lastname: Guerne
mesh_terms: D000209:Acute-Phase Proteins / Q000378:metabolism; D000210:Acute-Phase Reaction / Q000097:blood; D015703:Antigens, CD / Q000097:blood*; D001172:Arthritis, Rheumatoid / Q000097:blood* / Q000473:pathology; D004797:Enzyme-Linked Immunosorbent Assay; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein; D008180:Lupus Erythematosus, Systemic / Q000097:blood* / Q000473:pathology; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood*; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D012720:Severity of Illness Index; D012795:Sialoglycoproteins / Q000097:blood*; D013167:Spondylitis, Ankylosing / Q000097:blood* / Q000473:pathology
chemical_list: D000209:Acute-Phase Proteins; D015703:Antigens, CD; C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D012795:Sialoglycoproteins