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IL-23 is needed to protect mucosal surfaces from bacterial pathogens. Murphy and colleagues identify a Notch-2-dependent CD11b+ dendritic cell population that produces IL-23 and is required for survival after infection with Citrobacter.
The adaptor Nck is known for linking TCR signaling to cytoskeleton regulation. Batista and colleagues show that in B cells, Nck recruits the adaptor BCAP to the BCR to activate the PI(3)K pathway.
Failure to clear apoptotic cells can lead to autoinflammatory disease. Means and colleagues demonstrate that the receptor SCARF1 recognizes C1q-bound apoptotic cells, which leads to their clearance and prevents lupus-like symptoms.
The E3 ubiquitin ligases that modify the kinase RIP2 downstream of the receptor Nod2 remain unclear. Moynagh and colleagues show that Pellino3 ubiquitinates RIP2 for Nod2-induced activation of the transcription factor NF-κB.
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.