Anti-CarP antibodies in two large cohorts of patients with rheumatoid arthritis and their relationship to genetic risk factors, cigarette smoking and other autoantibodies

Ann Rheum Dis. 2014 Oct;73(10):1761-8. doi: 10.1136/annrheumdis-2013-205109. Epub 2014 May 8.

Abstract

Introduction: In rheumatoid arthritis (RA), several genetic risk factors and smoking are strongly associated with the presence of anticitrullinated protein antibodies (ACPA), while much less is known about risk factors for ACPA-negative RA. Antibodies against carbamylated proteins (anti-CarP) have been described in both ACPA-positive and ACPA-negative RA patients. In this study, we have analysed the relationships among anti-CarP antibodies, ACPA, genetic risk factors (HLA-DRB1 alleles and PTPN22) and smoking in RA.

Methods: Presence of antibodies to carbamylated fetal calf serum (CarP-FCS) and fibrinogen (CarP-Fib) was determined by inhouse ELISAs among RA cases in the Leiden Early Arthritis Clinic (n=846) and in the Swedish Epidemiological Investigation of Rheumatoid Arthritis (n=1985) cohorts. ORs for associations with different HLA-DRB1 alleles, PTPN22 genotypes and smoking were calculated separately for each cohort as well as in meta-analysis in RA subsets defined by the presence/absence of anti-CarP and anticyclic citrullinated peptide (anti-CCP) antibodies.

Results: In both cohorts, anti-CarP antibody positivity was mainly detected in the anti-CCP-positive population (49%-73%), but also in the anti-CCP-negative population (8%-14%). No associations between anti-CarP antibodies and HLA-DRB1 shared epitope alleles could be identified, while there were data to support an association between anti-CarP-FCS and HLA-DRB1*03. Further analyses did not reveal any specific associations of anti-CarP antibodies with other HLA-DRB1 alleles, PTPN22 genotypes or smoking.

Conclusions: Anti-CarP antibodies were present in both ACPA-positive and ACPA-negative RA. There were no significant associations among anti-CarP antibodies and HLA-DRB1 alleles, PTPN22 or smoking. These data suggest that different biological mechanisms may underlie anti-CarP versus anti-CCP antibody formation.

Keywords: Autoantibodies; Epidemiology; Gene Polymorphism; Rheumatoid Arthritis.

Publication types

  • Meta-Analysis
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Alleles
  • Arthritis, Rheumatoid / etiology
  • Arthritis, Rheumatoid / genetics
  • Arthritis, Rheumatoid / immunology*
  • Autoantibodies / blood*
  • Case-Control Studies
  • Cohort Studies
  • Female
  • Genetic Predisposition to Disease
  • Genotype
  • HLA-DRB1 Chains / genetics
  • Humans
  • Immunoglobulin G / blood
  • Male
  • Middle Aged
  • Muscle Proteins / immunology*
  • Nuclear Proteins / immunology*
  • Peptides, Cyclic / immunology
  • Protein Tyrosine Phosphatase, Non-Receptor Type 22 / genetics
  • Repressor Proteins / immunology*
  • Risk Factors
  • Smoking / adverse effects
  • Smoking / immunology*
  • Young Adult

Substances

  • ANKRD1 protein, human
  • Autoantibodies
  • HLA-DRB1 Chains
  • Immunoglobulin G
  • Muscle Proteins
  • Nuclear Proteins
  • Peptides, Cyclic
  • Repressor Proteins
  • cyclic citrullinated peptide
  • PTPN22 protein, human
  • Protein Tyrosine Phosphatase, Non-Receptor Type 22