Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Neutrophils can function as chief effector cells in inflammation but can also regulate excessive inflammatory responses by secreting anti-inflammatory cytokines. The acute-phase reactant SAA-1 seems to be pivotal in the control of such plasticity.
Human immunodeficiency virus type 1 (HIV-1) seems to avoid detection by nucleic acid sensors. This is probably due to the host exonuclease TREX1, which degrades HIV DNA generated during HIV-1 infection.
Induction of the microRNA miR-182 by interleukin 2 in helper T lymphocytes targets the transcription factor Foxo1 and promotes clonal expansion. Targeting this process opens new possibilities for adjuvancy, immunosuppression and anti-inflammatory therapeutics.
Complexities in sample handling, instrument setup and data analysis are barriers to the effective use of flow cytometry to monitor immunological parameters in clinical trials. The novel use of a central laboratory may help mitigate these issues.
IL-35 is an immunomodulatory cytokine secreted by regulatory T cells. Vignali and colleagues demonstrate that IL-35 also mediates the induction of a unique regulatory population that may underpin infectious tolerance.
The function of IL-37 remains elusive. Dinarello and colleagues find that IL-37 acts as a natural suppressor of innate inflammatory and immune responses.
Clonal expansion of helper T lymphocytes initially requires inactivation of the transcription factor Foxo1 by post-translational modifications. Mashreghi and colleagues now show in the late phase of clonal expansion, Foxo1 is inhibited post-transcriptionally by the microRNA miR-182.
IL-12 is believed to mediate antitumor activity via NK and TH1 cells. However, Becher and co-workers now show that IL-12 activates NKp46+ lymphoid tissue–inducer cells, which locally modify the tumor environment.
Foreign nucleic acids trigger innate immune sensors. Bowie and colleagues identify the PYHIN protein IFI16 as an innate duplex DNA sensor that triggers IFN-β production in a STING-TBK1-IRF3 signaling pathway.
How neutrophils differentiate into anti-inflammatory or proinflammatory effector cells is unclear. Cerundolo and colleagues now show that systemic serum amyloid A 1 controls the plasticity of neutrophil differentiation.
Many activating immunoreceptors are protein complexes in which ligand recognition and signaling functions are provided by separate modules. Wucherpfennig and co-workers report the nuclear magnetic resonance structure of the heterotrimeric DAP12-NKG2C receptor.
IAPP, a hormone secreted together with insulin and deposited in pancreatic islets in type 2 diabetes, can induce macrophage processing of interleukin 1 linked to beta-cell destruction in type 2 diabetes.
The regulation of gene expression through changes in chromatin structure is increasingly recognized as a chief component of activation of cells of the immune response. It now seems that histone demethylation of the promoter of the gene encoding the transcription factor IRF4 contributes to alternative macrophage activation.