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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 relationship between atopic dermatitis and air pollution has been long debated but has now been connected via the aryl hydrocarbon receptor and its control of skin innervation and the consequent triggering of an itch-scratch response.
The deubiquitinase USP15 acts with the ubiquitin ligase TRIM25 to activate a type I interferon response and exacerbate microbial and autoimmune neuroinflammation.
Different cellular sources and signaling mechanisms mediate the effects of IL-6 on the generation of pathogenic TH17 helper T cells and the suppression of Foxp3+ regulatory T cells.
Altered signaling via the T cell antigen receptor (TCR) promotes an adipose-tissue-like phenotype in invariant natural killer cells (iNKT cells) during thymic development and causes selective enrichment for iNKT cells in adipose tissues.
A surprising molecular mechanism underlying signal integration and programmed proliferation in adaptive immunity has been identified: the cell-cycle regulator Myc enables a lymphocyte to add up the strength of signals it receives and time its response accordingly.
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.
