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Modulation of integrin activation can contribute to regulation of inflammation. Arase and colleagues demonstrate that PILRα, an ITIM-containing inhibitory receptor, negatively regulates integrin activation and neutrophil infiltration during inflammation.
Activation of type I interferon by c-di-GMP and c-di-AMP depends on the adaptor STING. Cheng and colleagues show that these bacterial secondary messengers are detected by the helicase DDX41, which forms a complex with STING.
NK cell licensing is governed by the interaction of Ly49 receptors with peptide-MHC complexes. Smyth and colleagues show that the nonclassical MHC class I molecule H2-M3 can also license NK cell functional development.
The Igh locus undergoes a precise order of gene rearrangement during V(D)J recombination. Sen and colleagues show the recruitment of the RAG recombinase is confined to DJH junctions by highly localized epigenetic modifications.
The receptors for IL-2 and IL-15 share many characteristics, but mice deficient in either receptor have very different phenotypes. Garcia and colleagues present the quaternary structure of the complex of IL-15 and its receptor, as well as insights into its unique signaling properties.
The linear ubiquitination complex (LUBAC) is poorly understood in humans. Casanova and colleagues identify natural mutations in a component of human LUBAC and use this to dissect its function in vivo and in vitro.
Noncanonical RelB–NF-κB2 heterodimers function in homeostatic signaling. Hoffmann and colleagues show that RelB-p50 complexes, regulated by IκB, exist in dendritic cells and contribute to inflammatory gene expression via canonical NF-κB pathway activation.
The complement receptor CD46 and the Notch-Jagged system are important for the differentiation of helper T cells. Kemper and colleagues demonstrate that Jagged1 is a physiological ligand for CD46 and is critical for the generation of T helper type 1 cells in humans.
The deubiquitinating enzyme USP25 restricts ubiquitination of the adaptors TRAF5 and TRAF6 and signaling via interleukin 17 and thus joins several ubiquitin-modifying enzymes already known to regulate this biomedically important pathway.
Limiting immune responses is critical for protecting the host from harm. The p110δ isoform of the kinase PI(3)K acts as a balance between pro- and anti-inflammatory TLR4 signaling in dendritic cells.
The kinase TBK1 participates in signaling pathways that induce antimicrobial responses. TBK1 is also necessary for the suppression of excessive production of immunoglobulin A by accelerating destruction of the kinase NIK.
A fundamental mystery of the biology of germinal center B cells is why it seems that these rapidly dividing B cells lack expression of c-Myc, a transcriptional regulator intimately linked to cell metabolism and proliferation. This mystery has now been resolved.