In this respect, most interesting cells to study the methylation of the IL2RA gene promoter are regulatory T cells in which IL-2 signaling seems to be a major effector in the pathophysiology of T1D. However, since T cells represent 40-60% of WBC and regulatory T cells expressing IL2RA only 10% of peripheral CD4+ and,1% of CD8+, this was beyond the reach of our study. To get IL2RA expressing cells, large amounts of WBC can be freshly sorted, but this needs exceedingly large blood sample not accessible in clinical research in children or adolescents and was not feasible from our preexisting DNA bank. This is why, we confined our study to a subset of 8 healthy persons, in whom we found that the level of DNA methylation in the IL2RA promoter of regulatory T cells was lower than in other WBC while being correlated with methylation in other blood cells. Whether this has a functional meaning cannot be known from the current data. IL2RA is also expressed in a variety of hematopoietic cell types, including activated T and Blymphocytes, NK cells, monocytes and a subset of dendritic cells. In conclusion, the picture of genetic and epigenetic variation at a T1D risk locus was shown by the current study to be both entangled and complex. A given risk allele of a T1D associated SNP is associated with increased methylation at a risk CpG, while another risk allele of another T1D-associated SNP is associated with decreased methylation. The overall level of methylation of the risk CpG being increased in T1D patients, it is clear that the genetic influence of the studied SNPs was not the sole factor that could explain the AbMole Enoxacin hydrate changes in methylation observed in the T1D patients. Only 1.7% of the variance of methylation at CpG 2373 could be attributed to rs2104286 and 4.6% to rs11594656. This leaves a large contribution to influences from other genetic variants or environmental factors shaping the methylation of CpG throughout development. We do not think that the observed methylation changes in T1D could be attributed to the disease status, since they were independent from diabetes duration or HbA1c, although subtle T1D-associated environmental factors acting for example through dietary changes could be important in determining DNA methylation level in specific positions. The parasite and host factors that control the outcome of this infection are not well understood, although there is emerging evidence that host, parasite and environmental factors influence the outcome of infection. Alteration in the transcription of certain crucial genes is also likely to contribute to the outcome of infection. The latent period between infection and disease in humans suggests that the parasite adapts to the host via altered gene expression. This is best illustrated by the ability of E. histolytica to select for increased virulence of an axenic strain of E. histolytica by multiple rounds of passage through animals.