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TGF-β promotes the differentiation of TH-17 and regulatory T cells. Stockinger and colleagues show that TGF-β also directs differentiation of a unique interleukin 9–producing T cell subset.
TLR9 binds unmethylated CpG DNA and sends signals from endolysosomes. Ploegh and colloeagues find that cleavage mediated by endolysosomal cathepsins is required for TLR9 activation.
The E3 ubiquitin ligases Itch and Nedd4 target similar proteins in vitro. Oliver and colleagues find that unlike hyper-responsive Itch-mutant T cells, Nedd4-deficient T cells are hyporesponsive and contain excess Cbl-b.
In a variety of organisms, signals from the nervous system influence adaptive immunity. Tan and Kawli now show the importance of neuroendocrine inputs in the innate immunity of Caenorhabditis elegans to bacterial pathogens.
The transcriptional regulation of Il17 expression is not well understood. Strober and colleagues identify conserved noncoding sequences that, by a mechanism dependent on differential binding of Runx1 to RORγt and Foxp3, regulate Il17 expression.
The antigen-presenting abilities of plasmacytoid dendritic cells (DCs) are not well characterized. Villadangos and colleagues show that unlike conventional DCs, plasmacytoid DCs continue to synthesize and degrade MHC class II molecules, and thereby present endogenous viral antigen, after activation.
Some bacteria evade immune detection in the human respiratory tract. Slevogt and colleagues show that bacterial stimulation of the ITIM-containing CEACAM1 protein initiates signals that suppress TLR2-induced Akt activation and inflammation.
Activation of intracellular signaling pathways can result in MHC binding to and presentation of phosphorylated peptides. Engelhard and colleagues identify a unique phosphorylated peptide–MHC binding mode that allows solvent exposure of phosphorylated residues.
Plasmacytoid dendritic cells are best known as potent producers of type I interferon. Butcher and colleagues identify a subset of these cells, characterized by CCR9 expression, that can elicit tolerance in the gut.
Defective thymic egress in mice is associated with the peripheral T cell deficiency (Ptcd) locus. Cyster and colleagues find that the actin regulator coronin 1A is mutant in Ptcd and in an atypical patient with SCID.
Tumors often resist immune-mediated destruction because of the presence of suppressor cells. Lambris and colleagues show that activated complement C5a helps mediate this effect by recruiting myeloid suppressor cells to the tumor microenvironment.
Succinate is a Krebs cycle intermediate. Carballido and colleagues show that succinate released by necrotic cells also functions as an 'alarmin' by activating dendritic cells that express the succinate receptor GPR91.
Interleukin 4 (IL-4) drives T helper type 2 differentiation, whereas IL-2 augments Il4 chromatin accessibility. Leonard and colleagues now find that IL-2 also maintains the expression of Il4ra and other genes in T helper type 2–committed cells.
Interferon-γ (IFN-γ) is toxic to cells, yet IFN-γ-producing cells survive. Feng and colleagues show that expression of the GTPase Irgm1 in these cells confers protection against IFN-γ toxicity.
Virulent strains of Mycobacterium tuberculosis cause necrotic death of infected macrophages, which promotes bacterial dissemination. Remold and colleagues demonstrate that mycobacteria inhibit formation of the apoptotic envelope on macrophages, thus causing necrosis.
The transcription factor ThPOK is required for CD4+ T cell differentiation. Groups led by Taniuchi, Bosselut and Littman define distinct functions for ThPOK and other transcription factors in commitment versus specification of the CD4+ T cell lineage.
The C-type lectin family member Mincle is expressed mainly on macrophages. Saito and colleagues show that the nuclear protein SAP130, released by dead cells, is a ligand of Mincle that drives proinflammatory cytokine production by macrophages.
The transcription factor ThPOK is required for CD4+ T cell differentiation. Groups led by Taniuchi, Bosselut and Littman define distinct functions for ThPOK and other transcription factors in commitment versus specification of the CD4+ T cell lineage.
The transcription factor ThPOK is required for CD4+ T cell differentiation. Groups led by Taniuchi, Bosselut and Littman define distinct functions for ThPOK and other transcription factors in commitment versus specification of the CD4+ T cell lineage.
The mammalian target of rapamycin pathway regulates many essential cellular responses. Pulendran and colleagues show that this pathway is required for Toll-like receptor–mediated production of type I interferon by plasmacytoid dendritic cells.