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Starczynowski and colleagues show that overexpression of TRAF6 in HSCs induces ubiquitination of the RNA-binding protein hnRNPA1 and alternative splicing of Arhgap1, which accounts for the hematopoietic defects in myelodysplastic syndromes.
Gringhuis, Geijtenbeek and colleagues show that the RNA helicase DDX3 binds abortive HIV-1 RNA and induces type I interferon in dendritic cells, a process that is inhibited by the HIV-1-induced activation of kinase PLK1.
Natural killer T cells in the thymus are CD1d-restricted cells that are selected at the CD4+CD8+ double-positive stage and require a variety of transcription factors for their development. Orkin, Winau and colleagues show that the histone demethylase UTX serves an essential role in the transcriptional control of the thymic maturation of these cells through multiple epigenetic mechanisms.
Thymic regulatory T (Treg) precursors undergo a distinct developmental pathway. Sakaguchi and colleagues show the chromatin organizer Satb1 is required for establishing the super-enhancer chromatin landscape of Treg cell–specific signature genes before Foxp3 expression.
Sensors of RNA viruses trigger prion-like aggregation of the adaptor MAVS, which leads to antiviral responses. Gao and colleagues show that the E3 ligase TRIM31 positively regulates this process by K63-linked polyubiquitination of MAVS.
Various autoimmune diseases have sex-linked biases. Gudjonsson and colleagues find that the transcription factor VGLL3 is associated with a female-biased molecular signature linked to susceptibility to autoimmune disease.
Cornall and colleagues show that Themis2 interacts with the phospholipase PLC-γ2 and lowers the threshold for B cell activation by low but not high avidity antigens.
The phosphatase calcineurin targets NFAT transcription factors in T cells. Ashwell and colleagues show that calcineurin is recruited to the TCR signaling complex, where it reverses the inhibitory phosphorylation of the kinase Lck.
Abramson and colleagues show that the coordinated action of several transcriptional regulators, including Irf4, Irf8, Tbx21, Tcf7 and Ctcfl, acts on medullary-thymic-epithelial-cell-specific accessible regions in the locus encoding the transcriptional regulator Aire to control its expression.
The signaling adaptor TRAF1 is involved in TNFR-induced survival. Watts and colleagues demonstrate that TRAF1 also negatively regulates NF-κB activation by interfering with linear ubiquitination of the signaling subunit NEMO.
Korn and colleagues report that Sirpα+ dendritic cells trans-present the cytokine IL-6 to T cells through a process that requires its receptor IL-6Rα bound to dendritic cells and that trans-presentation is needed to generate pathogenic cells of the TH17 subset of helper T cells in vivo.
Lillemeier and colleagues describe a cycle of recruitment, activation and release of Zap70 kinase at phosphorylated T cell antigen receptors. According to this model, the receptor acts as a ‘catalytic unit’ that amplifies antigenic stimuli.
There are suspected links between air pollution and atopic dermatitis, but the mechanism has remained unclear. Yamamoto and colleagues demonstrate that air pollutants trigger activation of the aryl hydrocarbon receptor in the skin, hyperinnervation and an itch-scratch cycle that leads to atopic dermatitis.
Sant’Angelo and colleagues show that disruption of a hydrophobic patch in the T cell antigen receptor on natural killer T cells alters their development, which results in the selective accumulation of adipose-tissue-specific natural killer T cells.
TET proteins regulate 5-methylcytosine epigenetic marks, and thereby regulate chromatin accessibility. Rao and colleagues show that the combined loss of TET2 and TET3 in thymocytes skews development to iNKT17 cells as a result of upregulation of RORγt, which leads to lymphoproliferative disease and premature death.
Natural killer cells are a rapid source of the cytokine IFN-γ that influences ensuing immune responses. Schwab and colleagues report that gradients of the signaling lipid S1P regulate the positioning of natural killer cells in lymph nodes necessary for this response.
Krönke and colleagues show that the cytokine IL-23 controls the glycosylation profile and inflammatory activity of autoantibodies through control of sialyltransferase activity in plasma cells mediated by the TH17 subset of helper T cells.
Lymphocytes integrate multiple input signals to regulate the extent of their proliferative response. Hodgkin and colleagues demonstrate that the proto-oncoprotein Myc is a cell-intrinsic division timer.
The cytokine IL-18 can drive autoantibody production. Karlsson and colleagues show that such responses are limited by a three-way cellular interaction whereby splenic neutrophils activate both B cells and invariant natural killer T cells but the activated B cells are killed by FasL+ invariant natural killer T cells.
Fibroblastic reticular cells influence the function of lymphocytes in secondary lymphoid organs. Ludewig and colleagues demonstrate that they also specifically restrain the activation of group 1 innate lymphoid cells in the presence of microbial stimulation to prevent immunopathology.