New Study Reveals How Immune Response Impacts DNA Methylation

In a groundbreaking study published today, researchers shed light on the intricate relationship between immune activity and DNA methylation, a crucial process in gene regulation. The study, conducted on 190 individuals’ primary monocytes, delves into how inflammatory stimuli, particularly lipopolysaccharide (LPS), affect DNA methylation.

What the researchers found is fascinating: they observed that the impact of LPS on monocyte DNA methylation varies depending on the site, with demethylation occurring after hydroxymethylation. This discovery led to the identification of 7,359 high-confidence immune-modulated CpGs (imCpGs), which exhibit differences in genomic location and usage of transcription factors based on whether they experience a gain or loss in DNA methylation.

Of particular significance is the enrichment of demethylated imCpGs in enhancers, which are regions of DNA involved in enhancing gene expression. These imCpGs also align with genes associated with various diseases, notably cancer, suggesting a potential link between immune activity and disease development.

Furthermore, the study uncovered an intriguing association between DNA methylation and aging. Exposure to LPS for just 24 hours was found to induce approximately six months of epigenetic aging, directly linking innate immune activity with the aging process at the molecular level.

By integrating the changes in DNA methylation induced by LPS with genetic variation, the researchers identified 234 imCpGs that are under the control of local genetic factors. This finding opens up new avenues for understanding how genetic variation influences immune response and disease susceptibility.

Intriguingly, the study also revealed shared causal loci between LPS-induced DNA methylation changes and traits associated with human diseases. This suggests that certain genetic variants known to be linked to diseases may also play a role in modulating the formation of imCpGs in response to immune activity.

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