title: Lectin-reactive anti-α-gal in patients with Crohn's disease: correlation with clinical phenotypes.
abstract: BACKGROUND
  Patients with inflammatory bowel disease have higher proportions of immunoglobulin G (IgG) antibodies lacking N-galactose, also called agalactosyl IgG, in their serum. Such agalactosyl IgGs have been associated with disease activity and the immunogenicity of biologics. The aim was to describe the relationship between circulating levels of a subset of agalactosyl IgGs (anti-α-Gal) and Crohn's disease (CD) phenotypes.
  
  
  METHODS
  Prospectively collected serum samples of a well-characterized cohort of patients with inflammatory bowel disease and controls were used. Serum anti-α-Gal levels were measured by a high-affinity enzyme-linked immunosorbent assay and referenced to a standard control.
  
  
  RESULTS
  Serum samples from 167 subjects were tested; 62 with CD, 76 with ulcerative colitis, and 29 controls. Agalactosyl anti-α-Gal levels were significantly higher in active CD than in active ulcerative colitis (P = 0.0043) or healthy controls (P < 0.0001). Among patients with CD, agalactosyl anti-α-Gal levels were significantly higher in those with a history of arthritis, than those without (P = 0.0002), but lower in those taking immunomodulators (P = 0.03). There was no correlation between agalactosyl anti-α-Gal levels and indices of Crohn's severity, including C-reactive protein levels or Harvey-Bradshaw index. Patients who were primary or secondary nonresponders to infliximab had similar agalactosyl anti-α-Gal levels to clinical responders.
  
  
  CONCLUSIONS
  Patients with CD have greater amounts of agalactosylated anti-α-Gal antibodies in their serum, particularly in those with associated joint disease. This increase seems to be independent of indices of disease activity, but is influenced by immunomodulator use.
authors.affiliation: *Liver Disease Center, Beth Israel Deaconess Medical Center, Boston, Massachusetts; †Center for Inflammatory Bowel Disease, Beth Israel Deaconess Medical Center, Boston, Massachusetts; and ‡Department of Microbiology and Immunology, Drexel College of Medicine, Pennsylvania Biotechnology Center, Philadelphia, Pennsylvania.
authors.forename: Parham
authors.initials: P
authors.lastname: Safaie
authors.forename: Maggie
authors.initials: M
authors.lastname: Ham
authors.forename: Peter
authors.initials: P
authors.lastname: Kuang
authors.forename: Anand S
authors.initials: AS
authors.lastname: Mehta
authors.forename: Mengjun
authors.initials: M
authors.lastname: Wang
authors.forename: Adam S
authors.initials: AS
authors.lastname: Cheifetz
authors.forename: Simon
authors.initials: S
authors.lastname: Robson
authors.forename: Daryl
authors.initials: D
authors.lastname: Lau
authors.forename: Timothy M
authors.initials: TM
authors.lastname: Block
authors.forename: Alan C
authors.initials: AC
authors.lastname: Moss
mesh_terms: D000328:Adult; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D003093:Colitis, Ulcerative / Q000276:immunology* / Q000473:pathology; D003424:Crohn Disease / Q000276:immunology* / Q000473:pathology; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood*; D037102:Lectins / Q000276:immunology*; D008297:Male; D010641:Phenotype; D011379:Prognosis; D011446:Prospective Studies
chemical_list: D007074:Immunoglobulin G; D037102:Lectins; C064155:agalactosyl IGG; D002097:C-Reactive Protein