Epigenetic signature of human immune aging in the GESTALT study.

Age-associated DNA methylation in blood cells convey information on health status. However, the mechanisms that drive these changes in circulating cells and their relationships to gene regulation are unknown. We identified age-associated DNA methylation sites in six purified blood-borne immune cell types (naive B, naive CD4 and CD8 T cells, granulocytes, monocytes, and NK cells) collected from healthy individuals interspersed over a wide age range.

Cytomegalovirus infection reduced CD70 expression, signaling and expansion of viral specific memory CD8 T cells in healthy human adults.

Background: Cytomegalovirus (CMV) infection leads to effector memory CD8 T cell expansion and is associated with immune dysfunction in older adults. However, the molecular alterations of CMV-specific CD8 T cells in CMV infected healthy young and middle-aged adults has not been fully characterized.

Results: We compared CD8 T cells specific for a CMV epitope (pp65, NLV) and an influenza A virus (IAV) epitope (M1, GIL) from the same young and middle-aged healthy adults with serum positive for anti-CMV IgG.

DNA methylation signatures reveal that distinct combinations of transcription factors specify human immune cell epigenetic identity.

Epigenetic reprogramming underlies specification of immune cell lineages, but patterns that uniquely define immune cell types and the mechanisms by which they are established remain unclear. Here, we identified lineage-specific DNA methylation signatures of six immune cell types from human peripheral blood and determined their relationship to other epigenetic and transcriptomic patterns. Sites of lineage-specific hypomethylation were associated with distinct combinations of transcription factors in each cell type.