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The transcription factor Aire restrains the transcriptional duration and amplitude of tissue-specific self-antigens by opposing the activity of the chromatin remodeler Brg1—a process required for immune tolerance.
CD8+ tissue-resident memory T cells (TRM cells) in two mucosal tissues, the skin and the female reproductive tract, proliferate in situ to generate a secondary pool of TRM cells that does not exit into the circulation.
Detrimental levels of intracellular reactive oxygen species engage a caspase-independent and non-inflammatory cell death called ‘oxeiptosis’ that serves as an important mechanism in diminishing inflammation.
Turner and Díaz-Muñoz discuss the molecular mechanisms by which RNA-binding proteins modulate the diversity of the transcriptome and proteome in immune cells.
Gabrilovich and colleagues review the origin and nature of myeloid-derived suppressor cells, as well as their distinctive features and biological roles in cancer, infectious diseases, autoimmunity, obesity and pregnancy.
Crabtree and colleagues show that Aire has an intrinsic repressive function that restricts chromatin accessibility and restrains the amplitude of active transcription.
Yipp and colleagues report that depletion of B cells leads to the accumulation of aged polymorphonuclear cells in the lungs, which causes fibrotic interstitial lung disease.
Masopust and colleagues show that mucosal tissue-resident memory T cells proliferate in situ in response to local antigen and dominate the local recall response.
Mackay, Mueller and colleagues show that tissue-resident memory T cells proliferate in situ in response to local antigen and persist during subsequent antigen encounters.
The bacterial secondary messenger c-di-AMP can be sensed by cytosolic receptors to activate innate immunity. Fan and colleagues show the ER-associated protein ERAdP to be a high-affinity receptor for c-di-AMP, linking it to downstream inflammatory responses.
Klein and colleagues show, in a mouse model of West Nile virus–induced cognitive dysfunction, that neurogenesis is impaired by production of IL-1 from pro-inflammatory astrocytes.
Reactive oxygen species (ROS) are generated by cells during viral infection. Pichlmair and colleagues demonstrate a ROS-dependent form of cell death, ‘oxeiptosis’, that resembles apoptosis but uses a pathway distinct from all previously described death pathways.
A previously unknown role is identified for a pathway that involves major histocompatibility complex class I and an inhibitory receptor, LILRB1, that regulates the phagocytosis of cancer cells by macrophages and contributes to resistance directed against the signal-regulatory protein CD47.
Single-cell sequencing identifies novel subtypes of intestinal epithelial cells and their molecular signatures, which reveals new principles for gut homeostasis and the response to infection.