Genome-wide association studies have been tremendously successful in identifying 
genetic variants associated with complex diseases. The majority of association 
signals are intergenic and evidence is accumulating that a high proportion of 
signals lie in enhancer regions. We use Capture Hi-C to investigate, for the 
first time, the interactions between associated variants for four autoimmune 
diseases and their functional targets in B- and T-cell lines. Here we report 
numerous looping interactions and provide evidence that only a minority of 
interactions are common to both B- and T-cell lines, suggesting interactions may 
be highly cell-type specific; some disease-associated SNPs do not interact with 
the nearest gene but with more compelling candidate genes (for example, FOXO1, 
AZI2) often situated several megabases away; and finally, regions associated 
with different autoimmune diseases interact with each other and the same 
promoter suggesting common autoimmune gene targets (for example, PTPRC, DEXI and 
ZFP36L1).