shown to be different in the CPA group. The profiles were generated using MeDIP followed by hybridization to microarrays with probes placed at 100 bp-spacing starting from about −40 Kb before the transcription start site of each gene of interest to about 40 Kb after its transcription end site. Thus, the profiles included not only the promoters and bodies of these genes but also more distant sites in order to identify any genomic site with methylation levels altered in CPA individuals that might explain the previously observed lower cytokine levels. Differences between the CPA and control groups were found throughout each cytokine loci in both cell types analyzed (Table 1). In total, 48 differentially methylated regions associated with CPA (∼1000 bp, log2-fold >0.5, FDR <0.2) were identified in the cytokine loci, 20 in T cells and 28 in monocytes. Surprisingly, none of these were located in the promoters of the candidate cytokines, defined as the region from −2000 bp to +1000 bp of the transcription start site, although one differentially methylated region was found just outside the promoter (−2042 bp) of IL-6 (Figure 1). Two differentially methylated regions were found in the enhancer/insulator locus control region (LCR) of the IL-4
