title: [Fine specificity of anti-β2glycoprotein I antibodies in systemic autoimmune diseases is mostly directed against domain 1].
abstract: OBJECTIVE
  Anti-β2 GPI are a formal laboratory criterion for the antiphospholipid syndrome (APS). They were demonstrated to be a risk factor for thrombosis and fetal losses but can also be detected in patients with systemic autoimmune disease (SAD), in healthy adults individuals and pre-school children. It has been suggested that different subpopulations of anti-β2GPI may carry different pathogenetic potential: autoantibodies against Domain1 seem to be associated with thrombosis; autoantibodies against Domain4/5 have been identified in patients with non-thrombotic conditions.
  
  
  METHODS
  We studied 48 patients with SAD (32 systemic lupus erythematosus, 16 undifferentiated connettive tissue disease), 64 patients with APS, 57 one-year-old healthy children born to mother with SAD, 33 children with atopic dermatitis. All subjects were IgG anti-β2 GPI positive. The specificity of anti-β2 GPI was investigated using ELISA research products containing recombinant β2 GPI D1 and D4/5 antigens. Cut-off values are calculated as 95th percentile on 100 NHD. IgG anti-β2 GPI were tested at a validated home-made ELISA routinely performed in our laboratory. No thrombotic events were recordered in patients with SAD and in both groups of children.
  
  
  RESULTS
  Patients with SAD and APS showed prevalent reactivity for D1 while children in both groups preferentially recognize D4/5.
  
  
  CONCLUSIONS
  IgG anti-β2 GPI against D1 seem to cluster in patients with systemic autoimmune conditions. Their pathogenic potential in determine APS manifestations may be mitigated by adequate prophylaxis.
authors.affiliation: U.O. Reumatologia e Immunologia Clinica, A.O. Spedali Civili, Piazzale Spedali Civili 1, Brescia, Italia.
authors.forename: C
authors.initials: C
authors.lastname: Nalli
authors.forename: L
authors.initials: L
authors.lastname: Andreoli
authors.forename: M
authors.initials: M
authors.lastname: Motta
authors.forename: G L
authors.initials: GL
authors.lastname: Norman
authors.forename: Z
authors.initials: Z
authors.lastname: Shums
authors.forename: W L
authors.initials: WL
authors.lastname: Binder
authors.forename: M
authors.initials: M
authors.lastname: Nuzzo
authors.forename: M
authors.initials: M
authors.lastname: Frassi
authors.forename: A
authors.initials: A
authors.lastname: Lojacono
authors.forename: A
authors.initials: A
authors.lastname: Meini
authors.forename: V
authors.initials: V
authors.lastname: Medeghini
authors.forename: T
authors.initials: T
authors.lastname: Avcin
authors.forename: P L
authors.initials: PL
authors.lastname: Meroni
authors.forename: A
authors.initials: A
authors.lastname: Tincani
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000918:Antibody Specificity; D001323:Autoantibodies / Q000097:blood / Q000276:immunology*; D001324:Autoantigens / Q000737:chemistry / Q000276:immunology*; D001327:Autoimmune Diseases / Q000097:blood / Q000276:immunology*; D003240:Connective Tissue Diseases / Q000097:blood / Q000276:immunology; D003876:Dermatitis, Atopic / Q000097:blood / Q000276:immunology; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D007112:Immunity, Maternally-Acquired / Q000276:immunology; D007223:Infant; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000276:immunology; D008297:Male; D008875:Middle Aged; D018448:Models, Immunological; D011247:Pregnancy; D011248:Pregnancy Complications / Q000276:immunology; D017434:Protein Structure, Tertiary; D055815:Young Adult; D053482:beta 2-Glycoprotein I / Q000737:chemistry / Q000276:immunology*
chemical_list: D001323:Autoantibodies; D001324:Autoantigens; D053482:beta 2-Glycoprotein I