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Background  Genetic and epigenetic variability contributes to the susceptibility and pathogenesis of autoimmune diseases. T cells play an important role in several autoimmune conditions, including lupus, which is more common and more severe in people of African descent. To investigate inherent epigenetic differences in T cells between ethnicities, we characterized genome-wide DNA methylation patterns in naïve CD4+ T cells in healthy African-Americans and European-Americans, and then confirmed our findings in lupus patients.    Results  Impressive ethnicity-specific clustering of DNA methylation profiling in naïve CD4+ T cells was revealed. Hypomethylated loci in healthy African-Americans were significantly enriched in pro-apoptotic and pro-inflammatory genes. We also found hypomethylated genes in African-Americans to be disproportionately related to autoimmune diseases including lupus. We then confirmed that these genes, such as  IL32 ,  CD226 ,  CDKN1A , and  PTPRN2  were similarly hypomethylated in lupus patients of African-American compared to European-American descent. Using patch DNA methylation and luciferase reporter constructs, we showed that methylation of the  IL32  promoter region reduces gene expression in vitro. Importantly, bisulfite DNA sequencing demonstrated that  cis -acting genetic variants within and directly disrupting CpG sites account for some ethnicity-specific variability in DNA methylation.    Conclusion  Ethnicity-specific inherited epigenetic susceptibility loci in CD4+ T cells provide clues to explain differences in the susceptibility to autoimmunity and possibly other T cell-related diseases between populations.    Electronic supplementary material  The online version of this article (doi:10.1186/s13072-015-0037-1) contains supplementary material, which is available to authorized users.

Ethnicity-specific epigenetic variation in naïve CD4+ T cells and the susceptibility to autoimmunity