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Cancer can be associated with alterations in innate immunity. Gao et al. demonstrate that these alterations arise from immunomodulatory exosomes released by tumors, which then dampen the production of type I interferons by macrophages.
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.