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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.
Cells infected with human immunodeficiency virus type 1 do not produce type I interferon responses. Lieberman and colleagues report that the cytosolic exonuclease TREX1 prevents the accumulation of replication intermediates of this virus that could otherwise trigger intracellular sensors.
TGF-β signaling can promote the induction of regulatory T cells. Chi and colleagues show that the sphingosine 1-phosphate receptor S1P1 inhibits prolonged activity of the signal transducer Smad3 to block the generation of induced regulatory T cells, promoting TH1 differentiation instead.
Lymphocytes must rapidly scan lymph nodes for cognate antigens. Krummel and colleagues show that myosin IIA acts to optimize cell motility by regulating cell contacts through lymph node stromal environments.
Pancreatic islets in type 2 diabetes show characteristic deposition of the amyloid polypeptide IAPP. O'Neill and colleagues show that IAPP induces IL-1β production via the NLRP3 inflammasome, which leads to beta-cell destruction.
SLAM is best known for its homotypic costimulatory molecule functions. Terhorst and colleagues now demonstrate that it also acts as a sensor for Gram-negative bacteria and regulates the antibacterial response.
The role of caspase-12 in viral immunity has not been characterized yet. Fikrig and colleagues now show that it positively regulates the response to West Nile Virus through control of ubiquitinylation of the viral RNA receptor RIG-I.
The transcription factors Ikaros and Id2 regulate the development of both the natural killer and lymphoid tissue–inducer lymphoid lineages. Kaye and co-workers now show that the DNA-binding factor TOX is also required.
The proinflammatory cytokine IL-1β signals via a heterodimeric receptor composed of the receptor IL-1RI and the accessory protein IL-1RAcP. Wang and colleagues solve the ligand-receptor structure and explain how antagonist interactions differ.
Induced regulatory T cells help maintain peripheral tolerance. Flavell and colleagues show that the transcription cofactor Hopx is essential in maintaining the anergy and function of these cells.
Greater production of interleukin 17A is associated with severe asthma. Wills-Karp and colleagues show that the complement anaphylatoxins C3a and C5a have opposing roles in enhancing or suppressing IL-17a in allergic asthma.
Macrophages can be divided into two subsets, M1 and M2, which have crucial differences in their function. Akira and colleagues identify the histone demethylase Jmjd3 as a key factor in M2 development.
Allergies to nickel are the most frequent cause of contact hypersensitivity in industrialized countries. Goebeler and co-workers show that nickel induces an inflammatory response via direct activation of human Toll-like receptor 4.
MicroRNAs regulate many biological processes, including the development of cells of the immune response. Liu et al. demonstrate that a decrease in particular microRNAs prevents macrophage hyperactivation but primes their responsiveness to proinflammatory stimuli.
CD46 is best known as a regulator of complement function. Kemper et al. show that CD46 can switch inflammatory T cells into a regulatory mode and demonstrate the molecular details of this process.