title: A decrease in galectin-1 (Gal-1) levels correlates with an increase in anti-Gal-1 antibodies at the synovial level in patients with rheumatoid arthritis.
abstract: BACKGROUND
  Several studies have confirmed that galectin-1 (Gal-1) plays a role in controlling the immune response because of its pro-apoptotic effect. Although studies based on a rheumatoid arthritis (RA) mouse model have suggested a crucial role for Gal-1 in inflammation, clinical data are lacking. We have detected the presence of autoantibodies against galectins in blood, but their physiological meaning remains unknown.
  
  
  OBJECTIVE
  To compare plasma and synovial levels of Gal-1 in RA patients and in healthy controls, and correlate them with clinical parameters.
  
  
  METHODS
  Plasma and synovial (non-arthritic knee effusion) samples were collected from RA patients and healthy donors. All patients were receiving treatment with steroids and/or disease-modifying anti-rheumatic drugs (DMARDs). A blood sample was taken at a baseline visit to determine plasma anti-cyclic citrullinated peptide (anti-CCP) antibodies, tumour necrosis factor alpha (TNF-α), Gal-1, and anti-Gal-1 autoantibodies.
  
  
  RESULTS
  Although plasma levels of Gal-1 were similar in patients and controls, the concentration of Gal-1 was significantly reduced in the synovial fluid of patients with RA. This reduction was not correlated with TNF-α or C-reactive protein (CRP) levels. However, the decrease in synovial Gal-1 correlated with a significant increase in anti-Gal-1 autoantibodies and anti-CCP antibody titres, suggesting a physiological effect of autoantibodies limiting the amount Gal-1 and potentially blocking its biological effect in RA patients.
  
  
  CONCLUSIONS
  Gal-1 levels were significant reduced at the synovial level in RA patients, possibly as a consequence of the increase in anti-Gal-1 autoantibodies.
authors.affiliation: General Hospital of Cuernavaca, Faculty of Medicine, UAEM, Cuernavaca, Morelos, Mexico City, Mexico.
authors.forename: D
authors.initials: D
authors.lastname: Xibillé-Friedmann
authors.forename: C
authors.initials: C
authors.lastname: Bustos Rivera-Bahena
authors.forename: J
authors.initials: J
authors.lastname: Rojas-Serrano
authors.forename: R
authors.initials: R
authors.lastname: Burgos-Vargas
authors.forename: J L
authors.initials: JL
authors.lastname: Montiel-Hernández
mesh_terms: D000328:Adult; D018501:Antirheumatic Agents / Q000627:therapeutic use; D001172:Arthritis, Rheumatoid / Q000097:blood* / Q000188:drug therapy; D001323:Autoantibodies / Q000097:blood*; D016022:Case-Control Studies; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D037483:Galectin 1 / Q000097:blood*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010456:Peptides, Cyclic / Q000276:immunology; D013582:Synovial Fluid / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology; D055815:Young Adult
chemical_list: D018501:Antirheumatic Agents; D001323:Autoantibodies; D037483:Galectin 1; D010456:Peptides, Cyclic; D014409:Tumor Necrosis Factor-alpha; C487763:cyclic citrullinated peptide