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Using a gene-delivery system, we show that ectopic expression of interleukin 2 (IL-2) within reactive astrocytes stimulates brain-specific expansion of resident regulatory T cells. Such gene delivery protects against neuroinflammation in several mouse models of disease and injury, with potential implications for patients with traumatic brain injuries.
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.
Switching the CD4 and CD8 coreceptor proteins encoded in Cd4 and Cd8 loci results in a reversed T cell immune system, with CD4+ cytotoxic T cells and CD8+ helper T cells. Thus, whichever coreceptor is encoded in Cd4 promotes a helper lineage fate, and whichever is encoded in Cd8 promotes a cytotoxic lineage fate.
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.
The transcription factor TCF-1 has multiple roles during T cell development and in mature T cells. Gounari and Khazaie review the potential mechanisms by which TCF-1 regulates gene expression.
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.
A new genetic ‘recorder’ of long-term cell proliferation revealed substantial heterogeneity in the division history of central memory CD8+ T cells. Importantly, the extent of past proliferation was related to distinct transcriptional features and re-expansion potential, highlighting an unappreciated division of labor within the central memory T cell pool.
Systemic inflammatory responses generated by lipid-formulated RNA vaccines are driven by differential induction of pro- and anti-inflammatory interleukin-1 (IL-1) family members in mice and humans. Whereas RNA modifications can prevent these pro-inflammatory responses, certain lipid formulations used in the vaccines can induce IL-1-mediated innate immunity even in the absence of RNA.
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.
Cribriform plate-resident lymphatic endothelial cells respond to neuroinflammatory signals by inducing functional changes that enhance the capture and presentation of antigens from the cerebrospinal fluid and promote leukocyte interactions within the brain-draining lymphatics.
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.
The molecular basis for type I interferon (IFN)-mediated immunopathology is unclear. New data now identify the cGAS–STING pathway as a major driver of pathological type I IFN responses in COVID-19.
Alveolar macrophages (AMs), the resident macrophages of the lung, can be expanded ex vivo to generate large numbers of cells but show culture adaptations related to epigenetic and transcriptional changes. After transplantation into the lungs of mice, however, culture-expanded AMs lose these adaptations, fully restore in vivo identity and functionally reconstitute the AM pool.
Enormous progress has been made in the ten years since immune checkpoint blockade (ICB) was first approved for treating melanoma. Zappasodi and Huang review the current state of the art of ICB for melanoma and prospects for the future.
Increasingly, human monoclonal antibodies have been deployed against COVID-19, but combinations are typically needed for recognition of diverse viral variants. Bispecific antibodies could make the task of manufacturing and delivering combinations more efficient.
