PT  - JOURNAL ARTICLE
AU  - James Ding
AU  - Stephen Eyre
AU  - Jane Worthington
TI  - Genetics of RA susceptibility, what comes next?
AID  - 10.1136/rmdopen-2014-000028
DP  - 2015 Apr 01
TA  - RMD Open
PG  - e000028
VI  - 1
IP  - 1
4099  - http://rmdopen.bmj.com/content/1/1/e000028.short
4100  - http://rmdopen.bmj.com/content/1/1/e000028.full
SO  - RMD Open2015 Apr 01; 1
AB  - Genome-wide association studies (GWASs) have been used to great effect to identify genetic susceptibility loci for complex disease. A series of GWAS and meta-analyses have informed the discovery of over 100 loci for rheumatoid arthritis (RA). In common with findings in other autoimmune diseases the lead signals for the majority of these loci do not map to known gene sequences. In order to realise the benefit of investment in GWAS studies it is vital we determine how disease associated alleles function to influence disease processes. This is leading to rapid development in our knowledge as to the function of non-coding regions of the genome. Here we consider possible functional mechanisms for intergenic RA-associated variants which lie within lncRNA sequences.