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Inappropriate activation or inadequate regulation of CD4 +  and CD8 +  T cells may contribute to the initiation and progression of multiple autoimmune and inflammatory diseases. Studies on disease-associated genetic polymorphisms have highlighted the importance of biological context for many regulatory variants, which is particularly relevant in understanding the genetic regulation of the immune system and its cellular phenotypes. Here we show cell type-specific regulation of transcript levels of genes associated with several autoimmune diseases in CD4 +  and CD8 +  T cells including a  trans -acting regulatory locus at chr12q13.2 containing the rs1131017 SNP in the  RPS26  gene. Most remarkably, we identify a common missense variant in  IL27 , associated with type 1 diabetes that results in decreased functional activity of the protein and reduced expression levels of downstream  IRF1  and  STAT1  in CD4 +  T cells only. Altogether, our results indicate that eQTL mapping in purified T cells provides novel functional insights into polymorphisms and pathways associated with autoimmune diseases.

Pathogenic implications for autoimmune mechanisms derived by comparative eQTL analysis of CD4+ versus CD8+ T cells