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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.
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.
Specificity and function are the two main aspects that define T cell biology. A new report provides a technology that allows simultaneous assessment of both at the single-cell level.
The virome, increasingly recognized as a critical component of the mammalian microbiota, modulates host physiology. An antiviral treatment approach reveals that, via RIG-I signaling, the commensal virome is essential for the homeostasis of intestinal intraepithelial lymphocytes.
Acid sphingomyelinase deficiency, which prevents degradation of sphingomyelin (SM), causes lysosomal SM overload both in mice and in patients with Niemann–Pick disease A or B. Altered cellular SM homeostasis disrupts the development and function of natural killer T cells by obstructing the presentation of lipid agonists by CD1d molecules.
A report sheds new light on the molecular mechanisms responsible for the discrimination of self versus non-self TCR ligands and reveals the crucial role of the kinetics of LAT tyrosine phosphorylation in this.
Cyclic dinucleotides (CDNs) are potent activators of the innate immune sensor STING. The identification of a CDN importer sheds new light on the regulation of extracellular CDNs.
Chronic exposure to fungal antigen drives the development of two subsets of CD4+ TRM cells, distinguished by high or low expression of the integrin CD103, with opposing roles in inflammation-induced lung fibrosis.
Quantitative mass spectrometry applied to T cell activation reveals key insights into signal-transduction pathways. These data identify selective alterations in the concentration of proteins in activated T cells and detail previously undescribed protein–protein interactions.
A new study has identified various previously unknown mutations in the genes encoding human and mouse A20 that affect its phosphorylation and its function as an inhibitor of the transcription factor NF-κB, with implications for immunity and inflammatory disease.
Cellular metabolic screening identifies hyper-respiration, induced by gain-of-function mutations in the gene encoding succinate dehydrogenase, as a disease-driving immunometabolic trait of B cells from patients with primary antibody deficiency.
A specifically engineered Zika subunit vaccine based on the viral envelope protein mediates protective immunity in mice without inducing the cross-reactive antibodies responsible for antibody-dependent enhancement of infection with dengue virus.
Transcription-factor paralogs are not equivalent and serve distinct roles in immune cells. Analysis of the RUNX family of transcription factors reveals insights into the non-redundant roles of RUNX1 and RUNX3.
Therapeutic efficacy in inflammatory diseases is hampered by disease complexity. A monoclonal antibody that neutralizes IL-1R3, the common co-receptor of most inflammatory IL-1 cytokines, opens up new perspectives in effective disease management.
The transcription factor TOX epigenetically reprograms CD8+ T cells to drive T cell exhaustion during chronic infection and cancer. Although they are necessary for T cell persistence, these changes contribute to diminished anti-tumor function in exhausted cells.
The NFIL3–ZEB2–ID2 transcription-factor regulatory circuit switches the E protein–dependent +41 kb Irf8 enhancer in DC progenitors to the BATF3-dependent +32 kb Irf8 enhancer in mature cDC1s. Deletion of the cryptic +41 kb Irf8 enhancer impedes cDC1 development.
