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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.
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.
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.
Cao and colleagues found that the microRNA miR-1 promotes IFN-γ-mediated clearance of Listeria monocytogenes in macrophages by stabilizing the Stat1 mRNA through the degradation of the cytoplasmic long noncoding RNA Sros1.
Osteoclasts are a monocytoid cell with unique bone-remodeling capability. Ishii and colleagues demonstrate that the transcription factor FoxM1 is important for the differentiation of osteoclasts associated with pathological remodeling of the rheumatoid joint.
Savan and colleagues show that distinct isoforms of the RNA-binding protein ZAP function as an antiviral restriction factor or as an interferon-resolution factor, based on differences in their intracellular localization.
Fibroblastic reticular cells (FRCs) are dynamic regulators of lymphoid tissue structure. Turley and colleagues show FRCs also support activated T cells by producing IL-6, which confers an advantage to CD8+ T cell memory responses.
The impact of the commensal intestinal virome on health and immunity has been relatively little studied. Zhou and colleagues find that commensal viruses have an important function in maintaining intestinal intraepithelial lymphocytes, with implications for inflammatory bowel disease.
Niemann–Pick disease is characterized by the cellular accumulation of sphingomyelin. Blumberg and colleagues use both mouse models and materials from patients with Niemann–Pick disease to show that sphingomyelin accumulation inhibits CD1d-restricted NKT cell activation and development.
NK cells make an important contribution to the destruction of tumors. Wei and colleagues demonstrate that NK cells within the tumor microenvironment undergo mitochondrial fragmentation leading to impairment of their function and survival.
Zúñiga-Pflücker and colleagues show that Notch signaling is required before the thymic stages of T cell development to inhibit the myeloid lineage potential in thymus-seeding progenitors.
TCR ligation activates the tyrosine kinase ZAP-70 to phosphorylate the adapter LAT, which then coordinates TCR proximal signaling cascades. Weiss and colleagues show LAT-Y132 is critical to TCR ligand discrimination, as its phosphorylation represents a rate-limiting step in T cell activation due to a conserved glycine residue at position 131.
CRISPR activation (CRISPRa) can target select genes and, rather than being used to delete them, can be used to activate their expression. Chen and colleagues use a CRISPRa-based approach to drive the expression of multiple endogenous genes in tumors and presentation of the antigens encoded, thus enhancing antitumor immune responses.
Peyer’s patches (PPs) are sites of antibody production in the gut mucosa. Carroll and colleagues show the mechanosensory channel protein Piezo1 is required for the homeostatic maintenance of PPs. Specific loss of Piezo1 in FRCs disrupt PP structure and function, resulting in reduction of fecal IgA production and gut immunity.
Immature B cells expressing self-reactive BCRs induce anergy programs to promote tolerance. Busslinger and colleagues show that the transcription factor Ikaros enforces anergy by inducing transcription of negative-feedback regulators of the BCR and TLR–MyD88 pathways.
Marichal and colleagues show that lung neutrophils in mice exposed to three distinct pro-allergic conditions release neutrophil extracellular traps that potentiate allergen uptake by dendritic cells and type 2 allergic inflammation.
Gaudenzio and colleagues show that house dust mite extracts directly activate TRPV1+ sensory neurons, which promote allergic skin inflammation by inducing the degranulation of mast cells through the release of the neuropeptide substance P and activation of MRGPRB2.