PMID- 25775189
OWN - NLM
STAT- MEDLINE
DCOM- 20151215
LR  - 20210109
IS  - 1531-6963 (Electronic)
IS  - 1040-8711 (Linking)
VI  - 27
IP  - 3
DP  - 2015 May
TI  - New pathogenic insights into rheumatoid arthritis.
PG  - 249-55
LID - 10.1097/BOR.0000000000000174 [doi]
AB  - PURPOSE OF REVIEW: Rheumatoid arthritis (RA) is a heterogeneous chronic 
      immune-mediated inflammatory disease, associated with significant morbidity and 
      reduced life expectancy. Here, we review recent discoveries; particularly those 
      which have attempted to integrate genome-wide association studies (GWAS) with 
      biological pathways and cell types known to play a role in disease pathology in 
      order to expand our current understanding of the pathogenesis of RA. As the role 
      of stromal cells in the pathogenesis of RA has been reviewed in detail in Current 
      Opinions in Rheumatology, this area will not be covered in this review. RECENT 
      FINDINGS: Although our understandings of the pathogenic processes that drive 
      disease in RA remain incomplete, remarkable advances over the past year can be 
      highlighted. GWAS have raised awareness of important new risk loci with genes 
      that either are the targets of approved therapies for RA, or involve pathways for 
      drugs that could be repurposed from other disease indications such as cancer. 
      Furthermore, promising strides have been made in predicting the likelihood of 
      developing RA in those at risk using human leukocyte antigen (HLA), smoking, and 
      autoantibody status prediction models. These findings give a fresh insight into 
      RA pathogenesis and help identify new, or repurpose known therapeutic targets 
      from other disease areas. SUMMARY: The findings discussed in this review 
      underscore the progress made to date and the need for future studies, 
      investigating disease mechanisms in RA, with particular interest in at-risk RA 
      gene loci, their function in immune and stromal cells within the synovium, and 
      how they interact with environmental factors to initiate and perpetuate disease.
FAU - Jutley, Gurpreet
AU  - Jutley G
AD  - Rheumatology Research Group, Centre for Translational Inflammation Research, 
      University of Birmingham, Edgbaston, Birmingham, UK.
FAU - Raza, Karim
AU  - Raza K
FAU - Buckley, Christopher D
AU  - Buckley CD
LA  - eng
GR  - 19791/ARC_/Arthritis Research UK/United Kingdom
GR  - 19791/VAC_/Versus Arthritis/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - Curr Opin Rheumatol
JT  - Current opinion in rheumatology
JID - 9000851
RN  - 0 (Autoantibodies)
SB  - IM
MH  - Arthritis, Rheumatoid/*genetics/*immunology
MH  - Autoantibodies/*immunology
MH  - *Genetic Predisposition to Disease
MH  - *Genome-Wide Association Study
MH  - Humans
EDAT- 2015/03/17 06:00
MHDA- 2015/12/17 06:00
CRDT- 2015/03/17 06:00
PHST- 2015/03/17 06:00 [entrez]
PHST- 2015/03/17 06:00 [pubmed]
PHST- 2015/12/17 06:00 [medline]
AID - 10.1097/BOR.0000000000000174 [doi]
PST - ppublish
SO  - Curr Opin Rheumatol. 2015 May;27(3):249-55. doi: 10.1097/BOR.0000000000000174.