title: Cellular immune response to human cartilage glycoprotein-39 (HC gp-39)-derived peptides in rheumatoid arthritis and other inflammatory conditions.
abstract: OBJECTIVE
  To study the specificity of the peripheral blood mononuclear cell (PBMC) response to peptides derived from human cartilage glycoprotein-39 (HC gp-39) in patients with rheumatoid arthritis (RA) and the correlation between this response and disease activity.
  
  
  METHODS
  RA patients, patients with systemic lupus erythematosus (SLE), inflammatory bowel disease (IBD) or osteoarthritis (OA) and healthy controls were studied. All individuals were typed for HLA-DRB1 and their disease activity score was documented. Proliferation of PBMC was measured following incubation with five different HC gp-39-derived peptides, selected by the use of a DR4 (DRB1*0401) binding motif.
  
  
  RESULTS
  A proliferative response to one of the five peptides (peptide 259-271 at 10 microg/ml) was more often observed in RA patients than in healthy controls (P=0.001). RA patients who expressed DRB1*0401 more often showed a response against this peptide than RA patients who did not express this RA-associated haplotype. This response was not RA-specific since patients with IBD or OA also showed a response significantly more frequently than healthy controls (P:=0.02 and P=0.03 respectively). However, the level of the response against peptide 259-271 correlated with disease activity in RA patients but not in patients with IBD or SLE. Increased responses to HC gp-39 263-275 were found in patients with IBD or OA; a trend towards such a response failed to reach significance in RA patients in this study.
  
  
  CONCLUSIONS
  In RA patients as well as in patients with other inflammatory conditions, HC gp-39-derived peptides may be targets of the T-cell-mediated immune response. In the RA patient group the immune response to HC gp-39-derived peptide 259-271 correlated with disease activity.
authors.affiliation: Department of Rheumatology, Leiden University Medical Center, Leiden, The Netherlands.
authors.forename: K
authors.initials: K
authors.lastname: Vos
authors.forename: A M
authors.initials: AM
authors.lastname: Miltenburg
authors.forename: K E
authors.initials: KE
authors.lastname: van Meijgaarden
authors.forename: M
authors.initials: M
authors.lastname: van den Heuvel
authors.forename: D G
authors.initials: DG
authors.lastname: Elferink
authors.forename: P J
authors.initials: PJ
authors.lastname: van Galen
authors.forename: R A
authors.initials: RA
authors.lastname: van Hogezand
authors.forename: E
authors.initials: E
authors.lastname: van Vliet-Daskalopoulou
authors.forename: T H
authors.initials: TH
authors.lastname: Ottenhoff
authors.forename: F C
authors.initials: FC
authors.lastname: Breedveld
authors.forename: A M
authors.initials: AM
authors.lastname: Boots
authors.forename: R R
authors.initials: RR
authors.lastname: de Vries
mesh_terms: D054392:Adipokines; D000328:Adult; D000368:Aged; D001172:Arthritis, Rheumatoid / Q000276:immunology* / Q000473:pathology; D001324:Autoantigens / Q000032:analysis / Q000276:immunology; D000071451:Chitinase-3-Like Protein 1; D018450:Disease Progression; D005260:Female; D006023:Glycoproteins / Q000008:administration & dosage / Q000276:immunology* / Q000494:pharmacology; D006239:Haplotypes; D006801:Humans; D007111:Immunity, Cellular / Q000187:drug effects / Q000276:immunology; D037102:Lectins; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000008:administration & dosage / Q000276:immunology / Q000494:pharmacology; D013601:T-Lymphocytes / Q000276:immunology*
chemical_list: D054392:Adipokines; D001324:Autoantigens; C084533:CHI3L1 protein, human; D000071451:Chitinase-3-Like Protein 1; D006023:Glycoproteins; D037102:Lectins; D010446:Peptide Fragments