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Dick and colleagues map the transcriptional dynamics of human hematopoietic stem cells and early progenitor populations. The authors show that transcriptional programs are extensively shared, extend across lineage-potential boundaries and are not strictly lineage affiliated.
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.
The NLRP3 inflammasome is primarily known for producing inflammatory cytokines and inducing pyroptosis. Stuart and colleagues identify an additional role for NLRP3 in driving down the pH of phagosomes.
During chronic infection, pathogen-specific CD8+ T cells are thought to terminally differentiate into exhausted cells. However, Zehn and colleagues show that T cells with memory-like properties are generated during such infections.
The differentiation of αβ T cells is a complex process. Using data sets from the Immunological Genome Project, Benoist and colleagues identify candidate mediators of key transitions during thymocyte selection and maturation.
The Akt-mTOR axis influences cell activation, differentiation and metabolism. Jordan and colleagues show that thymic and inducible TH17 cells exhibit different requirements for mTORC1 and mTORC2 as well as Akt isoforms.
The mechanisms controlling maturation of mast cells toward an anaphylaxis-sensitive phenotype remain unclear. Murakami and colleagues show that PLA2G3, a mammalian homolog of anaphylactic bee venom phospholipase A2, regulates this process.
The developmental requirements of IL-17-committed γδ T cells remain unclear. Cyster and colleagues show that the transcription factor Sox13 is selectively required for the development of the Vγ4+ subset of γδ T cells.
The transcriptional circuitry that controls the differentiation of hematopoietic stem cells into cells of the immune system is only partially understood. Koller and colleagues use a computational algorithm to identify previously unknown differentiation stage–specific regulators of mouse hematopoiesis.
The roles of individual microRNAs in the CD8+ T cell response remain mostly unexplored. Katsikis and colleagues show that miR-155 regulates type I interferon responsiveness and CD8+ T cell responses to pathogens in vivo.
Innate lymphoid cells (ILCs) have been found in gut and lungs. Weninger and colleagues identify IL-13-producing ILCs in the skin, where they interact with mast cells and regulate allergic responses.
Chronic infections are commonly established in the liver. Knolle and colleagues show that cytotoxic T lymphocyte responses can be boosted by TLR-mediated induction of myeloid aggregates (iMATES).
T cell division is an intense metabolic process, and meeting its demands requires extensive metabolic reprogramming of the cell. Bensinger and colleagues demonstrate that SREBPs are critical for this reprogramming.
How hematopoietic stem cells coordinate self-renewal and differentiation remains unclear. Steidl and colleagues show that the transcription factor and chromatin remodeler Satb1 is required for their self-renewal.
Antibody production is the main effector function of B cells. Rawlings and colleagues show that Trypanosome cruzi induces rapid IL-17 production by B cells that is required for parasite control.
Tissue-resident effector memory T cells respond rapidly after reencountering antigen. Masopust and colleagues show that memory CD8+ T cells also induce the release of chemokines, then recruit more memory cells to the site of infection.
Inflammation needs to be tightly regulated to avoid immunopathology. Mallampalli and colleagues show that a system of F box proteins tunes proinflammatory signaling by degrading TRAF adaptor proteins.