Epigenetics in immune cells articles from across Nature Portfolio

Schwartz and colleagues show that T_H9 cells can respond to bystander cytokines IL-2 and IL-4 to induce antigen-independent expression of IL-9, promoting allergic inflammation. Il9 locus remodeling causes T_H9 cell instability, preventing antigen-independent activation in individuals who are nonallergic. Therapeutic targeting of the STAT5/STAT6 activation cascade may provide relief for patients with chronic allergy.

An integrated analysis uncovers transcriptional and epigenetic differences of human circulating memory T cell subsets and identifies unique transcription factor networks associated with memory subset differentiation.

An analysis of cis-regulatory domains (CRDs) among monocytes, neutrophils, and T cells derived from ChIP-seq peaks and methylation data suggests cell-type specific regulatory mechanisms of immunity.

The role of 3D genome organization is not well understood in the transcriptional regulation of dendritic cells. Here the authors show that activation of dendritic cells in vitro induces dynamic reprogramming of the chromatin looping and enhancer activity linked to changes in gene expression and implicates a role for the chromatin architecture protein CTCF in the inflammatory response of dendritic cells.

Th17 cells produce a range of characteristic Th17 type cytokines and express transcription factors governed by epigenetic regulation to engage the Th17 programme. Here the authors implicate the RNA 5- methylcytosine (m⁵C) methyltransferase Nsun2 in Th17 cells and the promotion of colitis in a murine model.

Murre and colleagues identify a specific enhancer, E34, within the Igk locus that is required for chromatin remodeling and repositioning to promote Rag-mediated Igkv7-33 V_κ-J_κ gene recombination, needed for generation of anti-phosphorylcholine-specific antibodies. Mice lacking E34 are more susceptible to Streptococcus pneumoniae infections.