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Vγ9Vδ2-expressing cells are a prominent γδ T cell population, but little is known about how they recognize antigens. De Libero and colleagues identify CD277 as an actual antigen-presenting molecule that binds stimulatory phosphorylated antigens.
Type I interferons regulate immune responses by signaling via heterodimeric IFNAR1-IFNAR2 complexes. Hertzog and colleagues reveal a unique IFN-β–IFNAR1 signaling complex that is IFNAR2-independent and modulates expression of a distinct set of interferon-inducible genes.
The signals controlling Treg cell homeostasis and survival are still being determined. Liston and colleagues demonstrate that peripheral Treg cells depend critically on IL-2 and the survival factor Mcl-1 but not on Bcl-2.
Exosomes have diverse physiological roles. Yuan and colleagues show that packaging of antiviral molecules into exosomes, followed by their release, is important in resistance to hepatitis viruses.
Lineage-commitment factors enforce irreversible loss of alternative lineage potentials during development. Grosschedl and colleagues show that EBF1 expression in committed pro-B cells suppresses T cell and innate lymphoid cell potential.
Particulate crystals can activate the NLRP3 inflammasome. Moore and colleagues show that the scavenger protein CD36 contributes to sterile inflammation via uptake of soluble cholesterol and amyloid peptides that nucleate into intracellular crystals.
The distal pathways for differentiation into monocytes and monocyte-derived macrophages are not fully elucidated. Feuerer and colleagues describe a clonogenic, monocyte- and macrophage-restricted progenitor derived from the macrophage–dendritic cell progenitor.
The robust generation of high-affinity antibodies by germinal center B cells requires help provided by TFH cells. Ansel and Xiao and their colleagues show that the microRNA family miR-17~92 regulates the differentiation and function of TFH cells.
The robust generation of high-affinity antibodies by germinal center B cells requires help provided by TFH cells. Ansel and Xiao and their colleagues show that the microRNA family miR-17~92 regulates the differentiation and function of TFH cells.
Cytokines that signal via IL-20R have been linked to autoinflammatory skin disease, but their role in infection is poorly understood. Datta and colleagues show that IL-20R signaling suppresses the production of IL-1β and IL-17 and dampens skin antibacterial responses.
T cells require CD28 costimulation for physiological activation. Malissen and colleagues show that the actin-uncapping protein Rltpr is needed to convey CD28 signaling by recruiting PKCθ and Carma1 to the immunological synapse.
Platelet activation contributes to blood coagulation. Kubes and colleagues show that platelets also act together with liver Kupffer cells to trap and eradicate blood-borne bacteria.
Liver X receptors (LXRs) are transcription factors that respond to sterols. Castrillo and colleagues identify a unique requirement for LXRα in the development of splenic marginal zone macrophages and their antibody responses to blood-borne antigen.
SOCS proteins suppress cytokine signaling by inhibiting activation of STAT signal transducers. Dong and colleagues show that the SOCS protein CIS is induced by IL-4 to control TH2 and TH9 helper T cell differentiation.
Moody and colleagues identify a subset of T cells with high affinity for complexes of CD1b and mycobacterial glycolipids, conserved TCRα use and biased TCRβ use. These 'GEM' T cells show interdonor conservation and proliferate after infection.
Additional editing activities for the cytidine deaminase AID beyond immunoglobulin-gene diversification have been proposed. Papavasiliou and colleagues now definitively show that antibody diversification is AID's sole physiological function in activated B cells.
The transcription factor GATA-3 is required for the differentiation of mature CD4+ T cells into TH2 cells. Wan and colleagues show that GATA-3 also controls the maintenance and proliferation of CD8+ T cells in the periphery.
CD52 is an important target for depleting antibodies; however, its physiological ligand and function have been unclear. Harrison and colleagues show that soluble CD52 is used by certain CD4+ cells to suppress target cells via the inhibitory receptor Siglec-10.
The mode by which NK cell receptors are bound to their ligands has been unclear. Rossjohn and colleagues show that the cytomegalovirus immunoevasin m157 binds the NK cell receptor Ly49 by its stalk region and not via the expected membrane-distal lectin domain.
How the adaptor Lat and the TCR come together after TCR triggering is not well understood. Hivroz and colleagues show that the vesicular protein VAMP7 is required for the recruitment of Lat-containing vesicles to TCR-activation sites.