demonstrate a preponderance of cell specific eQTL, as illustrated by systemic lupus erythematosus (SLE) for B-cells, while others traits show a predominance of monocyte-specific eQTL, as seen in ulcerative colitis (UC) (Figure 6). These diseases have contrasting and complex etiologies involving adaptive and innate immunity, the role of B-cells and autoantibody production being paramount in SLE, while in UC innate immunity involving dysregulated mucosal immunity and monocyte lineage cells are critically important. Our analysis defines a catalog of genes showing cell-specific or shared cis-eQTL for genetic variants implicated in many common diseases (Figure 6) (Supplementary Figure 15, Supplementary Table 6), facilitating the fine mapping and functional characterisation of specific genes and variants within GWAS disease intervals.
