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Cells of the immune system release cytokine 'factories' in the form of bioactive extracellular inflammasome assemblies. New findings by Franklin et al. and Baroja-Mazo et al. (pp 727 and 738; and News and Views by Broderick & Hoffman, p 698) identify extracellular functions of inflammasomes that are important for autoimmunity and the defense against pathogens. The original image shows the recruitment of neutrophils to injected extracellular specks of the adaptor ASC, which demonstrates their function as danger signals. Original image by Jacqueline M. Ratter. Artwork by Lewis Long.
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Inflammasome-driven inflammation extends into the extracellular space and to neighboring cells through the passive release of specks consisting of the adaptor ASC; this perpetuates the innate immune response and adds a dimension beyond interleukin 1 to autoinflammation.
Infection with an RNA virus induces the interferons IFN-β and IFN-λ via the adaptor MAVS located in mitochondria, while peroxisomal MAVS selectively activates an IFN-λ response.
Cells of the TH9 subset of helper T cells differentiated in the presence of interleukin 1β (IL-1β) produce large amounts of IL-9 and IL-21 in a manner dependent on the transcription factors STAT1 and IRF1 and exhibit potent anticancer effects.
Type III interferons have important antiviral functions, but they are poorly described compared to type I interferons. Kagan and colleagues demonstrate that type III interferons are induced on peroxisomes in response to a variety of viral triggers.
Various endogenous and pathogen-derived stimuli trigger the assembly of cytosolic multimolecular 'speck' platforms coordinated by the adapter ASC. Latz and colleagues demonstrate that ASC specks have extracellular functions that can prolong inflammation.
The NLRP3 inflammasome is involved in IL-1 production and pyroptosis. Pelegrín et al. demonstrate that it is also released extracellularly as a functional proinflammatory particle.
The kinase mTOR is important in lymphocyte bioenergetics but has not been examined in natural killer cells. Walzer and colleagues demonstrate that mTOR is key to sustaining the proliferation and effector function of these cells.
TH9 cells are associated with autoinflammatory diseases. Apetoh and colleagues demonstrate a molecular pathway which converts TH9 cells into potent anticancer cells.
Regulatory T (Treg) cells are needed to suppress autoreactive immune cell responses. Murre and colleagues show the transcriptional regulators Id2 and Id3 are necessary for proper Treg cell development, homing and maintenance.
Genome-wide epigenetic analyses can yield new insights into disease pathways. Vijayanand and colleagues mapped transcriptional enhancers in human T cells from healthy and asthmatic individuals and identify asthma-specific TH2 cell–associated enhancers.