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Using the Immunological Genome compendium, Brenner and colleagues shed light on the transcriptional programs that operate during the course of iNKT cell development and in peripheral CD4+ and CD4–iNKT cell subsets.
Gaus and colleagues show that the conformational states of the tyrosine kinase Lck intrinsically control its distribution and clustering at the plasma membrane.
Psoriasis is associated with heightened TH17 responses. Li and colleagues show that the IL-17R signaling adaptor Act1 requires the chaperone protein hsp90. Defective signaling leads to exuberant IL-22 production and enhanced disease.
ARIH2 is a RING-between-RING E3 ligase. Pellegrini and colleagues show that ARIH2 is needed to limit excessive NF-κB signaling in DCs. Loss of ARIH2 is associated with embryonic death due to excessive inflammatory responses.
The signals involved in coordinating the navigation of myeloid cells in tissues are incompletely understood. Massberg and colleagues show that NG2+ pericytes control the pattern and efficacy of interstitial leukocyte migration.
Chronic infections can result in harmful production of the proinflammatory cytokine IL-1 generated via the NLRP3 inflammasome. Sassetti et al. demonstrate that IL-1 activated by Mycobacteria results in nitrosylation and consequent regulation of the NLRP3 inflammasome.
Trex1 is a cytosolic exonuclease that limits sensing of intracellular DNA. Yan and colleagues show that Trex1 deficiency spontaneously heightens adaptor STING–dependent proinflammatory responses via a pathway involving regulation of lysosomal biogenesis.
Diseased host cells are eliminated more effectively when natural killer cells grow up in the presence of classical major histocompatibility complex (MHC) class I molecules. The nonclassical MHC class I molecule H2-M3 can exert an analogous effect.
Interleukin 2 (IL-2) and IL-15 use receptors with the same signaling subunits. New structural data show that the signaling complexes they form are topologically nearly identical, which suggests that other factors are responsible for the distinct signaling properties of these complexes.
Mathematical modeling shows that two members of the NF-κB family of transcription factors, RelB and p50, form heterodimers and participate in the canonical NF-κB pathway in dendritic cells.
Autoinflammation and immunodeficiency are rare in humans, but the rate of discovery of these conditions has increased. Three patients have now been characterized in whom deficiency in HOIL-1, a component of the LUBAC complex, leads to these conditions.
Bacterial cyclic dinucleotides are recognized by the innate immune system, and this leads to the induction of type I interferons. The mammalian helicase DDX41 directly binds cyclic dinucleotides and mediates the signaling pathway to the induction of type I interferons.