title: Soluble TRAIL concentrations are raised in patients with systemic lupus erythematosus.
abstract: BACKGROUND
  Increased apoptosis may induce autoimmune conditions. Apoptosis is induced by binding of death receptor ligands, members of the tumour necrosis factor (TNF) superfamily, to their cognate receptors. The Fas-Fas ligand pathway has been studied extensively in relation to systemic lupus erythematosus (SLE). However, other death pathways are also considered important. TNF related apoptosis inducing ligand (TRAIL), another ligand of the TNF superfamily, induces apoptosis in sensitive cells.
  
  
  OBJECTIVE
  To assess soluble (s) TRAIL concentrations in sera of SLE patients.
  
  
  METHODS
  40 SLE patients were studied (20 with active and 20 with inactive disease). Serum sTRAIL concentrations were measured by a solid phase sandwich enzyme linked immunosorbent assay. Levels in SLE patients were compared with those in patients with rheumatoid arthritis (n = 20), Wegener's granulomatosis (n = 20), and healthy controls (n = 20).
  
  
  RESULTS
  Mean (SEM) serum sTRAIL concentration in SLE patients (936.0 (108.2) pg/ml) was higher than in healthy controls (509.4 (33.8) pg/ml; p<0.01) or in disease control patients with rheumatoid arthritis (443.8 (36.1) pg/ml, p<0.001) or Wegener's granulomatosis (357.1 (32.2) pg/ml; p<0.001). The mean serum sTRAIL concentration was 1010.2 (168.0) pg/ml for patients with inactive disease and 861.8 (138.7) pg/ml for those with active disease. sTRAIL values were not correlated with specific manifestations of the disease, such as leucopenia or lymphopenia, or with SLE disease activity index.
  
  
  CONCLUSIONS
  Serum sTRAIL concentrations are increased SLE patients. This seems to be disease specific and could indicate a role for TRAIL in SLE pathophysiology.
authors.affiliation: Department of Clinical Immunology University Hospital Groningen, PO Box 30.001, 9700 RB Groningen, Netherlands.
authors.forename: M N
authors.initials: MN
authors.lastname: Lub-de Hooge
authors.forename: E G E
authors.initials: EG
authors.lastname: de Vries
authors.forename: S
authors.initials: S
authors.lastname: de Jong
authors.forename: M
authors.initials: M
authors.lastname: Bijl
mesh_terms: D000328:Adult; D000368:Aged; D017209:Apoptosis; D051017:Apoptosis Regulatory Proteins; D001172:Arthritis, Rheumatoid / Q000097:blood; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods; D005260:Female; D014890:Granulomatosis with Polyangiitis / Q000097:blood; D006801:Humans; D008024:Ligands; D008180:Lupus Erythematosus, Systemic / Q000097:blood*; D008297:Male; D008562:Membrane Glycoproteins / Q000097:blood*; D008875:Middle Aged; D012720:Severity of Illness Index; D012995:Solubility; D053221:TNF-Related Apoptosis-Inducing Ligand; D014409:Tumor Necrosis Factor-alpha
chemical_list: D051017:Apoptosis Regulatory Proteins; D008024:Ligands; D008562:Membrane Glycoproteins; D053221:TNF-Related Apoptosis-Inducing Ligand; C505653:TNFSF10 protein, human; D014409:Tumor Necrosis Factor-alpha