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Interleukins 4 and 13 are critical for responses to helminthes. Locksley and colleagues use genetically engineered reporter mice to assess the temporal and spatial production of these cytokines in vivo.
Invariant NKT cells elicit the rapid release of cytokines. Two papers by Leadbetter and Vinuesa and colleagues show that these cells can also provide direct help to B cells to elicit rapid antibody responses.
Invariant NKT cells elicit the rapid release of cytokines. Two papers by Leadbetter and Vinuesa and colleagues show that these cells can also provide direct help to B cells to elicit rapid antibody responses.
The generation of reactive oxygen species needs to be carefully controlled to prevent tissue injury. Malik and colleagues identify a negative feedback mechanism for such production involving the cation channel TRPM2.
Type 1 interferon limits virus replication. Lang and colleagues show that expression of Usp18 in metallophilic macrophages results in less interferon responsiveness, which allows locally restricted virus replication and the induction of adaptive immune responses.
The generation of certain gut innate lymphoid cell (ILC) populations requires the aryl hydrocarbon receptor (AHR). Colonna and colleagues show that the induction of Notch expression by AHR is required for the development of interleukin 22–producing NKp46+ ILCs.
The NF-κB transcription factor family comprises five distinct proteins. Bulyk and colleagues show that homo- and heterodimeric forms of NF-κB recognize distinct κB sites; this introduces additional specificity to NF-κB gene regulation.
The transcription factor STAT5 can activate or repress gene expression depending on whether binding of dimer or tetrameric STAT5 occurs. Tetrameric STAT5 recruits the chromatin modifier Ezh2 to silence gene expression.
Improper termination of inflammatory signals can contribute to tumorigenesis. Cyld and Itch form an ubiquitin-editing complex that cooperatively downregulates the kinase Tak1 and thereby attenuates downstream activation of the transcription factor NF-κB.
Natural killer T cells (NKT cells) recognize lipid-based antigens presented by CD1d. The mammalian glycolipid β-glucosylceramide, a ubiquitous self antigen for NKT cells, is upregulated by microbial danger signals, which leads to activation of NKT cells in the absence of foreign glycolipid antigen.
Two studies identify a tissue-autonomous innate immune mechanism whereby infection provokes epithelial cells to produce IL-17C that engages an epithelial receptor composed of IL-17RA and IL-17RE chains, which promotes host defense and immune activation.
Becoming covered in platelets rescues complement-opsonized blood-borne bacteria from rapid clearance by macrophages and redirects them to dendritic cells. Although this allows priming of T cells and the generation of immune memory, bacteria can exploit this route as a beachhead and disseminate throughout host tissues.