title: Increased levels of soluble TNF-like cytokine 1A in ankylosing spondylitis.
abstract: OBJECTIVE
  To determine the expression of soluble TNF-like cytokine 1A (sTL1A), a new member of the TNF superfamily, in patients with AS.
  
  
  METHODS
  Seventy-five consecutive patients with AS [61 males, mean (S.D.) age: 47.2 (15.5) years, disease duration: 20.3 (13.9) years] were included in this study. Forty-four patients were anti-TNF treatment naïve, whereas the remaining patients were on infliximab (n = 21), adalimumab (n = 3) or etanercept (n = 7). The patients' perceived disease activity was recorded by BASDAI and AS DAS using serum CRP levels (ASDAS-CRP), whereas functional status was assessed by BASFI and measurements of spinal mobility (AS Metrology). Serum concentrations of TL1A were measured by ELISA. Twenty-five age- and sex-matched healthy individuals served as controls.
  
  
  RESULTS
  Anti-TNF treatment-naïve patients demonstrated a 2.6-fold higher sTL1A average value [mean (s.e.m.) 581 (157.5) pg/ml] compared with healthy controls [226.7 (48.24) pg/ml, P = 0.042]. The sTL1A levels of anti-TNF-treated patients [178 (42)] were significantly lower than anti-TNF treatment-naïve patients (3.3-fold decrease, P = 0.0038) and comparable to those of healthy controls. No significant association was found between sTL1A level and functional status (BASFI score, AS Metrology parameters) or CRP measured in the same sera; however, a positive correlation was observed between individual levels of sTL1A and both BASDAI (P = 0.008) and ASDAS-CRP (P = 0.058) scores suggesting that sTL1A levels may reflect disease activity in patients with AS.
  
  
  CONCLUSIONS
  TL1A is up-regulated in AS, associates with disease activity and is influenced by anti-TNF treatment, suggesting that TL1A may be of pathogenic and potentially of therapeutic importance in AS patients.
authors.affiliation: First Department of Propaedeutic and Internal Medicine, Medical School, University of Athens, Athens, Greece.
authors.forename: Maria
authors.initials: M
authors.lastname: Konsta
authors.forename: Giorgos
authors.initials: G
authors.lastname: Bamias
authors.forename: Maria G
authors.initials: MG
authors.lastname: Tektonidou
authors.forename: Panayiotis
authors.initials: P
authors.lastname: Christopoulos
authors.forename: Alexios
authors.initials: A
authors.lastname: Iliopoulos
authors.forename: Petros P
authors.initials: PP
authors.lastname: Sfikakis
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D018501:Antirheumatic Agents / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D012720:Severity of Illness Index; D013167:Spondylitis, Ankylosing / Q000097:blood* / Q000188:drug therapy; D053380:Tumor Necrosis Factor Ligand Superfamily Member 15 / Q000097:blood* / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors; D015854:Up-Regulation; D055815:Young Adult
chemical_list: D018501:Antirheumatic Agents; D015415:Biomarkers; C117026:TNFSF15 protein, human; D053380:Tumor Necrosis Factor Ligand Superfamily Member 15; D014409:Tumor Necrosis Factor-alpha