Experiments in mice have shown than an enzyme that repairs broken DNA inside the nucleus also has a central role in the innate immune system because it is able to detect foreign DNA outside the nucleus.

A transmembrane protein uses distinct mechanisms to regulate the movement of specific toll-like receptors-key immune system components involved in detecting pathogens-to their final locations inside cells.

A key activator of Ras signaling adopts an autoinhibited, dimeric conformation that is activated by membrane and calcium binding.

The sequencing of microbial genomes reveals that the presence of a particular microbial species in the gut may increase the risk of the autoimmune disease rheumatoid arthritis.

Apoptotic cells release molecules to recruit macrophages, but do not cause inflammation because they also secrete AMP that functions as a ‘calm down’ signal.

Using mice expressing a Bcl-2 mutant protein to suppress multiple central tolerance pathways, it is shown that central tolerance is crucial for preventing autoimmunity.

A chemical biology approach has identified the kinase DYRK1A as a new regulator of the inflammatory response.

Global epigenetic perturbations and accumulation of RNA:DNA hybrids are two novel hallmarks of the lupus-like inflammatory disorder Aicardi-Goutières syndrome.

There is limited epigenetic conservation of lineage-specific DNA elements in Treg cells, and genetic variation in Treg cell specific enhancers is associated with autoimmune disease.

The ubiquitin ligase ROQUIN cross-talks with cellular metabolic signals to generate protective T cell-dependent antibody responses.