PMID- 28451788
OWN - NLM
STAT- MEDLINE
DCOM- 20180326
LR  - 20181113
IS  - 1863-2300 (Electronic)
IS  - 1863-2297 (Print)
IS  - 1863-2297 (Linking)
VI  - 39
IP  - 4
DP  - 2017 Jun
TI  - The role of autoantibodies in the pathophysiology of rheumatoid arthritis.
PG  - 437-446
LID - 10.1007/s00281-017-0627-z [doi]
AB  - Rheumatoid arthritis (RA) is an autoimmune disease characterized by joint 
      inflammation. The presence of autoantibodies in the sera of RA patients has 
      provided many clues to the underlying disease pathophysiology. Based on the 
      presence of several autoantibodies like rheumatoid factor (RF), 
      anti-citrullinated protein antibodies (ACPA), anti-carbamylated protein 
      antibodies (anti-CarP), and more recently anti-acetylated protein antibodies RA 
      can be subdivided into seropositive and seronegative disease. The formation of 
      these autoantibodies is associated with both genetic and environmental risk 
      factors for RA, like specific human leukocyte antigen (HLA) alleles and smoking. 
      Autoantibodies can be detected many years before disease onset in a subset of 
      patients, suggesting a sequence of events in which the first autoantibodies 
      develop in predisposed hosts, before an inflammatory response ensues leading to 
      clinically apparent arthritis. Research on the characteristics and effector 
      functions of these autoantibodies might provide more insight in 
      pathophysiological processes underlying arthritis in RA. Recent data suggests 
      that ACPA might play a role in perpetuating inflammation once it has developed. 
      Furthermore, pathophysiological mechanisms have been discovered supporting a 
      direct link between the presence of ACPA and both bone erosions and pain in RA 
      patients. In conclusion, investigating the possible pathogenic potential of 
      autoantibodies might lead to improved understanding of the underlying 
      pathophysiological processes in rheumatoid arthritis.
FAU - Derksen, V F A M
AU  - Derksen VFAM
AD  - Department of Rheumatology, Leiden University Medical Center, C1-R-041, 
      Albinusdreef 2, PO Box 9600, 2300 RC, Leiden, the Netherlands.
FAU - Huizinga, T W J
AU  - Huizinga TWJ
AD  - Department of Rheumatology, Leiden University Medical Center, C1-R-041, 
      Albinusdreef 2, PO Box 9600, 2300 RC, Leiden, the Netherlands. 
      T.J.W.Huizinga@lumc.nl.
FAU - van der Woude, D
AU  - van der Woude D
AD  - Department of Rheumatology, Leiden University Medical Center, C1-R-041, 
      Albinusdreef 2, PO Box 9600, 2300 RC, Leiden, the Netherlands.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20170427
PL  - Germany
TA  - Semin Immunopathol
JT  - Seminars in immunopathology
JID - 101308769
RN  - 0 (Autoantibodies)
RN  - 0 (Autoantigens)
SB  - IM
MH  - Animals
MH  - Arthritis, Rheumatoid/*etiology/metabolism/pathology
MH  - Autoantibodies/*immunology
MH  - Autoantigens/immunology
MH  - *Autoimmunity
MH  - Environment
MH  - Gene-Environment Interaction
MH  - Genetic Predisposition to Disease
MH  - Humans
MH  - Microbiota/immunology
MH  - Risk Factors
MH  - Signal Transduction
PMC - PMC5486798
OTO - NOTNLM
OT  - ACPA
OT  - Autoantibodies
OT  - Pathophysiology
OT  - Rheumatoid arthritis
EDAT- 2017/04/30 06:00
MHDA- 2018/03/27 06:00
PMCR- 2017/04/27
CRDT- 2017/04/29 06:00
PHST- 2017/04/01 00:00 [received]
PHST- 2017/04/10 00:00 [accepted]
PHST- 2017/04/30 06:00 [pubmed]
PHST- 2018/03/27 06:00 [medline]
PHST- 2017/04/29 06:00 [entrez]
PHST- 2017/04/27 00:00 [pmc-release]
AID - 10.1007/s00281-017-0627-z [pii]
AID - 627 [pii]
AID - 10.1007/s00281-017-0627-z [doi]
PST - ppublish
SO  - Semin Immunopathol. 2017 Jun;39(4):437-446. doi: 10.1007/s00281-017-0627-z. Epub 
      2017 Apr 27.