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The inclusion of the transcription factor Ikaros in the NuRD chromatin-remodeling complex regulates both the targeting and activity of the NuRD complex in lymphocytes, thereby influencing developmental gene-expression programs.
Lifting the protective shield provided by the type I interferon system selectively in CD169+ splenic macrophages enforces localized viral replication. Such controlled release of virus amplifies adaptive antiviral immune responses.
Harnessing invariant natural killer T cells can boost various immune responses. Two studies now shed light on the direct interaction between those cells and B cells that induce strong primary B cell responses.
The transmigration of effector T lymphocytes is critical to adoptive immune response. The rules for the migration of effector T cells are now reported to be distinct from those that apply to naive and memory T cells.
The transcription factor STAT5 can activate or repress gene expression depending on whether binding of dimer or tetrameric STAT5 occurs. Tetrameric STAT5 recruits the chromatin modifier Ezh2 to silence gene expression.
Improper termination of inflammatory signals can contribute to tumorigenesis. Cyld and Itch form an ubiquitin-editing complex that cooperatively downregulates the kinase Tak1 and thereby attenuates downstream activation of the transcription factor NF-κB.
Natural killer T cells (NKT cells) recognize lipid-based antigens presented by CD1d. The mammalian glycolipid β-glucosylceramide, a ubiquitous self antigen for NKT cells, is upregulated by microbial danger signals, which leads to activation of NKT cells in the absence of foreign glycolipid antigen.
Two studies identify a tissue-autonomous innate immune mechanism whereby infection provokes epithelial cells to produce IL-17C that engages an epithelial receptor composed of IL-17RA and IL-17RE chains, which promotes host defense and immune activation.
Becoming covered in platelets rescues complement-opsonized blood-borne bacteria from rapid clearance by macrophages and redirects them to dendritic cells. Although this allows priming of T cells and the generation of immune memory, bacteria can exploit this route as a beachhead and disseminate throughout host tissues.
Type 2 cytokine–producing innate lymphoid cells are present in human and mouse lungs, where they contribute to both type 2 immune responses and tissue repair.
How the kinase PKC-θ is targeted to the immunological synapse and is activated once there remains unclear. A targeting motif in PKC-θ and the previously unsuspected kinase GLK identified in two separate papers now explains this.
The kinase LRRK2 is a risk factor for inflammatory bowel disease. New data show that LRRK2 blocks the transport of NFAT to the nucleus and that LRRK2 deficiency results in enhanced susceptibility to experimental colitis in mice.
The antiviral factor APOBEC3G upregulates the expression of ligands for the activating receptor NKG2D via DNA damage induced by the viral protein Vpr in cells infected with human immunodeficiency virus. The virus overcomes greater susceptibility to natural killer cell–mediated lysis by targeting APOBEC3G for degradation.
T cell tolerance is essential to the prevention of autoimmunity. The ubiquitin E3 ligase Peli1 acts as a negative regulator of T cell activation and contributes to the maintenance of self-tolerance.
ASC has emerged as an adaptor for inflammasome sensors in cells of the innate immune response. New inflammasome-independent roles have been identified for ASC in the control of adaptive immunity; these include the post-transcriptional regulation of cytoskeletal rearrangements.
The sensing of pathogen-associated DNA in the cytoplasm is an important trigger of host-defense responses that include the production of type I interferon. A new study suggests that the DExDc helicase DDX41 may function in dendritic cells as a DNA sensor to activate STING-dependent innate immune responses.
In addition to its recognized function as an enzyme that catalyzes tryptophan, indoleamine 2,3-dioxygenase (IDO) acts as an intracellular signal transducer, in response to transforming growth factor-β (TGF-β), to induce a stably regulatory phenotype in plasmacytoid dendritic cells.
Tuberins, the tumor-suppressor proteins that regulate signaling via the kinase mTOR, now emerge as essential enforcers of T cell quiescence that promote survival.
Proinflammatory signaling by the interleukin 17 receptor requires the adaptor Act1. Two studies identify an additional function for Act1 and identify new participants that regulate the inflammatory effects of IL-17.
