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Foxp3 protein complexes orchestrate the transcriptional network of regulatory T cells. The Foxp3 interactome is now identified and may act as a genetic switch that controls the differentiation of regulatory T cells.
The activation of T cells requires the entry of calcium ions through the plasma membrane. A study now identifies a voltage-gated sodium channel as being essential for the sustained entry of calcium needed for the developmental process of positive selection.
The characteristics of the tumor microenvironment vary widely. New work shows that after tumor-associated expression of the receptor TIM-3 by dendritic cells, TIM-3 inhibits the antitumor efficacy of DNA vaccines and chemotherapy by binding to the damage-associated molecular pattern molecule, HMGB1.
The mechanism by which γδ T cells are triggered to respond to stress elicited by infection or malignancy has remained a mystery. New data identify endothelial protein C receptor as a stress ligand for γδ T cells that is induced by cytomegalovirus infection.
Structural studies identify considerable differences in the recognition of CD1d-lipid complexes by the TCRs of type II and type I (invariant) natural killer T cells.
The transcription factor Aiolos is upregulated in T lymphocytes in a manner dependent on the transcription factors STAT3 and AhR and leads to epigenetic silencing of the gene encoding interleukin 2. This acts as a cell-intrinsic safeguard mechanism for the differentiation of helper T cells into the TH17 subset.
Substantial depletion of Langerhans cells leads to their replenishment by bone marrow–derived precursors that access the epidermis through hair follicles, a site of crucial chemokine production.
The sensing of viral infection by the innate immune system is dominated by the recognition of nucleic acids. New data now demonstrate that the fusion of viral and target-cell membranes leads to the activation of an immune response dependent on the adaptor STING.
Most myeloid cells express the growth-factor receptor CSF1R. Recognition of interleukin 34 by CSF1R is required for the development of tissue-resident Langerhans cells and microglia, which explains the independence of their growth from CSF1.
Antiviral innate immunity often has deleterious effects on the course of bacterial infection. Activation of the transcription factor IRF3 induced by the recognition of double-stranded RNA by RIG-I-like receptors suppresses the Toll-like receptor–induced expression of interleukins 12 and 23 and antibacterial responses.
The cellular mechanism by which the cytokine TGF-β maintains the homeostasis of mature T cells and prevents the emergence of severe lethal lymphoproliferative disease has remained obscure. It is now shown that TGF-β restrains the homeostatic T cell proliferation driven by self ligands from erupting into overt autoimmunity.
'Elite controllers' of human immunodeficiency virus (HIV) maintain a long-term disease-free status after infection with HIV. A comparison of elite controllers and people who progress to disease after infection with HIV now suggests that clonotypic profiles of HIV-specific CD8+ T cells may underlie elite control.
The role of T cells in providing help to B cells is well established; however, the converse—that B cells provide signals to help initiate T cell–mediated immunity—is less well appreciated. New data now show B cells modulate the earliest stages of T cell activation in a T helper type 2 response.
