title: Antielastin B-cell and T-cell immunity in patients with chronic obstructive pulmonary disease.
abstract: BACKGROUND
  Antielastin autoimmunity has been hypothesised to drive disease progression in chronic obstructive pulmonary disease (COPD). The proposed mechanism is currently disputed by conflicting data. The authors aimed to explore antibody responses against elastin in a large and extensively characterised COPD population and to assess elastin-specific peripheral T-cell reactivity in a representative subgroup.
  
  
  METHODS
  Antielastin antibodies were analysed with indirect ELISA on the plasma of 320 patients with COPD (Global Initiative for Chronic Obstructive Lung Disease 1-4) and 143 smoking controls. In a second group of 40 patients with COPD and smoking controls, T-cell responses against extracellular matrix (elastin, collagen I and collagen V) were determined with enzyme-linked immunosorbent spot (EliSpot) (interferon γ (IFNγ) and interleukin-2) on peripheral blood mononuclear cells and compared with the responses of 11 never-smoking controls.
  
  
  RESULTS
  Antielastin antibody titres were not elevated in patients with COPD compared with smoking controls and even decreased significantly with increasing severity of COPD (p<0.001). Lower antielastin antibody titres were also found in a subgroup of patients with CT-proven emphysema. Elastin-specific INFγ-mediated T helper 1 responses could not be revealed in smoking subjects with and without COPD. Collagen I-mediated T-cell responses were also absent, which contrasted with a significant increased anticollagen V response in the smoking controls and patients with COPD compared with the never smokers (p=0.008). Collagen V-mediated T-cell responses could not discriminate between patients with COPD and smoking controls.
  
  
  CONCLUSIONS
  A systemic immune response against elastin could not be identified in patients with COPD. By contrast, collagen V-mediated autoimmunity was increased in the subgroup of smokers and may potentially contribute to the pathogenesis of COPD.
authors.affiliation: Laboratory of Pneumology, Respiratory Medicine, University of Leuven, Onderwijs en Navorsing 1 bus 706, Herestraat 49, Leuven 3000, Belgium.
authors.forename: Manuela
authors.initials: M
authors.lastname: Rinaldi
authors.forename: An
authors.initials: A
authors.lastname: Lehouck
authors.forename: Nele
authors.initials: N
authors.lastname: Heulens
authors.forename: Renaud
authors.initials: R
authors.lastname: Lavend'homme
authors.forename: Vincent
authors.initials: V
authors.lastname: Carlier
authors.forename: Jean-Marie
authors.initials: JM
authors.lastname: Saint-Remy
authors.forename: Marc
authors.initials: M
authors.lastname: Decramer
authors.forename: Ghislaine
authors.initials: G
authors.lastname: Gayan-Ramirez
authors.forename: Wim
authors.initials: W
authors.lastname: Janssens
mesh_terms: D000368:Aged; D001323:Autoantibodies / Q000097:blood*; D015551:Autoimmunity / Q000276:immunology; D001402:B-Lymphocytes / Q000276:immunology*; D024062:Collagen Type V / Q000276:immunology; D004549:Elastin / Q000276:immunology*; D005109:Extracellular Matrix / Q000276:immunology; D005260:Female; D005541:Forced Expiratory Volume / Q000502:physiology; D006801:Humans; D007111:Immunity, Cellular; D008297:Male; D008875:Middle Aged; D029424:Pulmonary Disease, Chronic Obstructive / Q000276:immunology* / Q000503:physiopathology; D012907:Smoking / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*; D014797:Vital Capacity / Q000502:physiology
chemical_list: D001323:Autoantibodies; D024062:Collagen Type V; D004549:Elastin