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In airway epithelial cells, exposure to allergen proteases induces the stress granules-mediated transfer of IL-33 from the nucleus to the cytoplasm and extracellular release through gasdermin D pores containing a newly described active fragment.
Extrathymic MHCII+Rorc+ Aire-expressing cells that share characteristics with type 3 innate lymphoid cells (ILC3s) internalize C. albicans and present its antigens, priming the development of Candida-specific TH17 cells.
Lymphocyte activation gene 3 (LAG3) is an important checkpoint inhibitor molecule of immunotherapeutic interest. New crystal structures of LAG3 provide important insight into its molecular architecture, laying the groundwork for future basic and applied investigations.
Regulatory T cells that express high levels of IL-1R and ICOS display transcriptional features of antigen specificity, are highly suppressive and distinguish tumors from non-malignant inflamed tissues
Inflamed tissue has a special milieu, with hypoxia, high levels of metabolites from anaerobic glycolysis, and acidosis. Stimulation of a proton-activated receptor, TDAG8 (GPR65), in T cells has an important role in inflammatory bowel disease by balancing pro- and anti-inflammatory signals.
Broadly protective antibodies to SARS-CoV-2 inform vaccine improvements and are directly used for treatment and prevention. New technologies are enabling the recovery of thousands of antibody examples, and workflows to rapidly identify the most potent examples are accelerating discovery.
Hypoxia alters populations of monocytes and macrophages during acute respiratory distress syndrome leading to persistent inflammation, a process that can be reversed by therapeutic administration of CSF1.
The dynamic changes in immune cell infiltration that accompany glioblastoma (GBM) progression remain obscure. Single-cell RNA sequencing and flow cytometry are now used to deconstruct the tumor immune microenvironment of early- and late-stage GBMs.
Inflammasomes function as immune-signaling platforms that assemble following pathogen detection. Direct binding of a viral protein to NLRP1 and the disruption of a previously unknown autoinhibitory NRLP1 complex drive the activation of the NLRP1 inflammasome independently of the proteasome.
Ectopic expression of IL-2 in the central nervous system (CNS) is sufficient to create an organ-restricted niche for tissue-resident regulatory T cells that support re-establishment of homeostasis after multiple types of tissue injury in the CNS.
Basophils are type 2 immune response cells, but they have also been associated with fibrosis. New data indicate that proximal tubule cells exert profibrotic effects by recruiting IL-6-producing basophils into the kidneys.
The activation of the noncanonical NLRP3 inflammasome can be elicited by the interaction and interdependent activation of caspase-11 and NLRP3 that follows coincident cytosolic detection of lipopolysaccharide and bacterial mRNA from live Gram-negative bacteria.
A role for mitochondrial ATP that leads to phosphocreatine and the subsequent generation of cytosolic ATP via creatine kinase B is now proposed in the activation of the NLRP3 inflammasome.
LAG3 interferes with TCR signaling by lowering the pH in the vicinity of the TCR and inducing dissociation of the key signaling kinase Lck from the co-receptors CD8 and CD4.
A genetic recorder of T cell replicative history identifies fewer accumulated divisions in a subset of CD8+ central memory T cells that shows stem-cell-like quiescence and superior recall capacity.
mRNA vaccines such as those used to prevent COVID-19 owe part of their success to methylation that masks immunostimulatory properties of the mRNA, but the immunological mechanisms of adjuvanticity are unclear. Two new studies reveal distinct mechanisms for innate sensing of this hidden adjuvant.
The formation of a provisional matrix is required for the onset of tissue repair. New research shows that neutrophils carry pre-existing matrix across organs into wounds, promoting fibroblast activation and scar formation.
B-cell-derived acetylcholine initiates a circuit that prompts bone marrow stromal cells to secrete factors that restrain the blood-forming activity of hematopoietic stem cells in response to cardiovascular dysfunction.
Targeting the post-translational modification enzyme QPCTL prevents the protection of CCL2 and CCL7 from N-terminal degradation, inactivates their chemotactic function and limits the recruitment of pro-tumoral macrophages.
