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A genome-wide screening of functionally active enhancers, combined with analyses of chromatin features, transcription factor binding and gene expression, reveals general principles of gene regulatory networks in activated B cells.
Radiation therapy has for decades been a standard form of treatment for many cancers. A Review by Galluzzi and colleagues explores the effects of radiation therapy in the context of the immune response.
Belz and colleagues show that the enteric neuron-derived neuropeptide VIP signals though its receptor VIPR on ILC3s to regulate the cyclic production of IL-22 in response to food intake.
Singh and colleagues leverage genome-wide assays to identify functionally active enhancers that are present in naive and lipopolysaccharide-activated B cells by FAIRE–seq, STARR–seq and Hi-C structural interactome analyses and identify additional transcription factors that regulate gene expression modules.
Pasare and colleagues describe an inflammasome-independent, TNFR–Fas–caspase-8-dependent pathway of IL-1β production triggered by cognate interactions between effector CD4+ T cells and mononuclear phagocytes.
IL-33, an IL-1 family member, plays dual roles as an intracellular transcription factor and as an extracellular alarmin of tissue damage. Verginis and colleagues identify a cell-intrinsic role for nuclear IL-33 stabilizing Treg cell suppressor function in tumor environments.
The International Mouse Phenotyping Consortium (IMPC) aims to identify the function of all protein-coding genes in the mouse genome. Hayday and colleagues leverage 530 knockout lines from the IPMC to develop the 3i Project, which immunophenotypes mice and leads to the identification of new and unexpected gene influences on immune function and on the structural organization of the immune system.
Progress in understanding the rare disease Langerhans cell histiocytosis has stimulated immersive meetings occurring annually over a 30-year period that bring together clinicians, scientists and patients in a unique collaboration.
IL-33 is shown to play a cell-intrinsic role in maintenance of the functional identity of regulatory T cells in the tumor microenvironment. Genetic inhibition of IL-33 potentiates the therapeutic effect of checkpoint inhibitor immunotherapy in a melanoma mouse tumor model.
NLRP3-driven sterile inflammation facilitates the pathogenesis of various human inflammatory diseases. New work identifies apolipoprotein C3 as an endogenous NLRP3 agonist that promotes sterile inflammation and organ damage.
Hypoxia and acidity in the tumor microenvironment promote resistance to immunotherapy. Hypoxia upregulates multiple immunoinhibitory pathways, including VISTA, and acidity enables VISTA to interact with PSGL-1 to inhibit immune activation selectively in the acidic tumor microenvironment.
Overabundance of apolipoprotein C3 (ApoC3) is associated with atherosclerosis. Speer and colleagues demonstrate that ApoC3 activates the NLRP3 inflammasome via a non-canonical pathway contributing to inflammation and development of atherosclerosis.
Croker and colleagues show that the phosphatase Ptpn6 functions to suppress neutrophil cell death pathways and IL-1 release, thereby limiting autoinflammatory responses.
Oxidized host-derived phospholipids such as oxPAPC can play important roles in atherosclerosis. Zanoni and colleagues demonstrate that oxPAPC generates a distinctive metabolic and hyperinflammatory profile in macrophages that can drive atherosclerosis in mice.
