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Noncanonical RelB–NF-κB2 heterodimers function in homeostatic signaling. Hoffmann and colleagues show that RelB-p50 complexes, regulated by IκB, exist in dendritic cells and contribute to inflammatory gene expression via canonical NF-κB pathway activation.
The complement receptor CD46 and the Notch-Jagged system are important for the differentiation of helper T cells. Kemper and colleagues demonstrate that Jagged1 is a physiological ligand for CD46 and is critical for the generation of T helper type 1 cells in humans.
Lineage development is accompanied by specification of gene expression. Murre and colleagues show that during B cell development, many genes relocate in the nucleus, driven by chromatin-looping interactions with transcription factors.
How IL-17 signaling is regulated remains poorly understood. Dong and colleagues identify the ubiquitin-specific protease USP25 as a negative regulator of IL-17-mediated signaling and inflammation.
Signaling through toll-like receptors induces cytokines and type I interferon. Moynagh and colleagues show that the E3 ubiquitin ligase Pellino3 specifically represses the expression of type I interferon in response to TLR3 activation.
By comparing gene-expression profiles, Randolph and colleagues distinguish different types of macrophages and pinpoint the differences between macrophages and dendritic cells.
How isotype-specific immunoglobulin production is regulated is largely unknown. Sun and colleagues show that the kinase TBK1 acts as a negative regulator of IgA class switching by attenuating NIK-mediated NF-κB signaling.
TLR4 signaling shifts from plasma membrane TIRAP-MyD88–mediated pathways to endosomal TRAM-TRIF–mediated signaling. Vanhaesebroeck and colleagues show that the kinase PI(3)K p110δ is required for TLR4 internalization and degradation of TIRAP.
Successful pathogens can overcome innate immune defenses. Ge and colleagues show that Tir protein expressed by enteropathogenic Escherichia coli is injected into host cells, where it interferes with adaptor TRAF6–dependent signaling.
The regulator c-Myc is well known for controlling cell growth but, paradoxically, evidence for its involvement in germinal centers has proven elusive. Rajewsky and colleagues show that it is essential for their development and maintenance.
The molecular control of germinal center selection is still being determined. Dalla-Favera and colleagues show that the cell-cycle regulator c-Myc is essential for B cell selection and reentry into the germinal center.
Hematopoietic stem cells must be shielded from toxic and inflammatory insults to ensure lifelong blood cell production. Lapidot and colleagues identify a rare bone marrow macrophage population that protects hematopoietic stem cells.
Exposure to interleukin 23 (IL-23) is required for the induction of pathogenic TH17 cells. Kuchroo and colleagues show that IL-23-dependent induction of the cytokine TGF-β3 produces a molecular signature characteristic of highly pathogenic TH17 cells.
Transcription factor Foxp3 is essential for the development and function of regulatory T cells, but it does not act in isolation. Benoist and colleagues identify a quintet of factors that facilitate transcriptional regulation by Foxp3.
'Lymphoid priming' in human bone marrow is traditionally thought to begin with the expression of CD10 on CD34+ progenitors. Crooks and colleagues now demonstrate lymphoid priming in a subset of CD10–CD34+ progenitors that are CD62Lhi.
The role of type I interferon in bacterial infection is poorly understood. Sad and colleagues demonstrate that Salmonella-triggered production of type I interferon induces macrophage necroptosis, evasion of the immune response and dissemination of bacteria.
The transcription factor Foxp3 is essential for the function of regulatory T cells. Rudensky and colleagues show Foxp3 participates in large protein complexes that regulate gene expression of many of these components in self-reinforcing networks.
Innate immune responses influence the composition of gut microbiota. Fu and colleagues show that weight gain incurred with high-fat diets is dependent on intact lymphotoxin signaling that regulates IL-23 and IL-22 production.
Lanier and colleagues systematically define the transcriptome of mouse natural killer cells in several contexts, including activation states and relative to all other lymphocyte and myeloid populations profiled by the Immunological Genome Project consortium.
Van Gisbergen and colleagues report that Hobit, a homolog of the transcription factor Blimp-1, controls the maintenance of mature mouse natural killer T cells and regulates their effector functions in a species-specific way.