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A hallmark of systemic lupus erythematosus is the production of type I interferons in response to immunocomplexes containing self DNA from dead cells and DNA-specific IgG. Sanjuan and colleagues find that IgE specific for self DNA also exacerbates this disease.
T cells proliferate in response to cues provided by antigen-presenting cells or high concentrations of cytokines. Krummel and colleagues reveal a distinct requirement for the cytoskeletal protein septin 7 for cytokine-driven bystander T cell proliferation.
PTEN functions as a tumor suppressor. Guo and colleagues now find PTEN also serves a critical role in antiviral innate immunity by inducing the production of type I interferon.
Sumolyation regulates wide-ranging biological processes, but its influence on innate immunity is unclear. Amigorena and colleagues show that sumoylation negatively regulates interferon-β expression and anti-viral immunity.
NEK7 is a serine-threonine kinase linked to mitosis. Beutler and colleagues show that NEK7 is required for assembly of the NLRP3 inflammasome and restricts NLRP3 activation to interphase of the cell cycle.
Macrophages densely populate the arterial wall, yet their origin and homeostasis are poorly understood. Robbins and colleagues show that arterial macrophages arise from CX3CR1+ embryonic precursors and adult bone marrow–derived monocytes that colonize the tissue immediately after birth.
Ectopic lymphoid structures develop at sites of chronic inflammation and are generally thought to be beneficial in the control of cancer. Pikarsky and colleagues show that these structures can instead nurture liver tumor progenitor cells.
The lipid S1P confers signals that regulate leukocyte trafficking. Schwab and colleagues generate mice that can faithfully report the bioavailability of S1P within tissues and reveal how S1P gradients are shaped in the spleen.
Holtzman and colleagues identify PARP9-DTX3L as an E3 ubiquitin ligase complex that interacts with STAT1 to modify chromatin accessibility for expression in interferon-stimulated genes and to target viral proteases for degradation.
Stress can induce expression of norepinephrine, which can enhance neuroinflammation. Shaked, Hedrick and colleagues show that the transcriptional repressor Nr4a1 limits this stress-induced response by suppressing expression of tyrosine hydroxylase required for the synthesis of norepinephrine.
Antigen-activated B cells differentiate into plasmablasts or germinal center B cells that undergo further affinity maturation. Singh and colleagues identify the antagonistic roles of transcription factors IRF4 and IRF8 that establish these opposing cell fates.
The molecular details of the control of TCR signaling are still being determined. Cao and colleagues report that the E3 ligase Nrdp1 negatively regulates activity of the signaling kinase Zap70 selectively in CD8+ T cells.
Little is known about the phosphatases involved in the control of TH17 cells. Yin and colleagues demonstrate that the phosphatase DUSP2 targets the transcription activator STAT3 to regulate the differentiation and function of TH17 cells.
The function of group 3 innate lymphoid cells (ILC3 cells) is still being determined. Vivier and colleagues describe the development of ILC3 subsets and show that NCR+ ILC3 cells are not needed to control infection with Citrobacter rodentium in the presence of an intact T cell compartment.
Mucosal surfaces often represent the first point of entry for pathogens. Paludan and colleagues demonstrate that disruption of the mucus itself can initiate a hyperacute innate immune response that precedes even the production of type I interferons.
The signals that negatively regulate group 2 innate lymphoid cells are incompletely understood. Moro and colleagues show that interferons and IL-27 restrain the function and proliferation of these cells in vitro and in vivo through a mechanism dependent on the transcription factor STAT1.
Dysregulation of group 2 innate lymphoid cells has been linked to virus-induced asthma. Fritz and colleagues demonstrate that deficiency in signaling via type I interferons in these cells can lead to dysregulated type 2 immunity during respiratory viral infection.
Group 3 innate lymphoid cells have low expression of the transcription factor GATA-3. Zhu and colleagues show that despite its low expression, GATA-3 is essential for the homeostasis, further maturation and effector function of lineage-committed group 3 innate lymphoid cells.
Memory TH2 cells are rapidly recruited to tissues after exposure to stimulatory ligands. McKenzie and colleagues demonstrate that ILC2s have an essential role in facilitating TH2 cell memory responses in lung, skin and gut.
Glucose availability is limiting in tumor environments. Zou and colleagues show that reduced glycolytic metabolism in T cells within tumors suppresses expression of the methyltransferase EZH2, which limits production of antitumor effector molecules and enhances T cell apoptosis.