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Liston and colleagues design a gene-delivery system to specifically target astrocytes in the central nervous system to express IL-2 and thereby expand/maintain Treg cells to suppress neuroinflammation.
Exhausted T cells are associated with inefficient viral clearance, tumor immunity and response to immunotherapy. Here the authors show CD8+ T cells in the pancreatic islets have a LAG3-promoted ‘restrained’ phenotype resembling exhausted cells but maintain effector functions, and LAG3 expression limits pathology in the nonobese diabetic mouse model of type 1 diabetes.
Liang and colleagues show that the ORF45 protein from the Kaposi’s sarcoma-associated herpesvirus activates NLRP1 by binding to its Linker1 region through a mechanism distinct from the previously described, host protease DPP9-dependent mechanism of NLRP1 activation.
How the immune system responds to epithelial cancers beyond neoantigen-driven adaptive immunity is poorly understood. Kansler et al. reveal an innate immune surveillance response mediated by cytotoxic ILC1 sensing of cancer cell-expressed IL-15.
How fibrosis and inflammation are integrated is not entirely clear. Here the authors show that profibrotic proximal tubular cells in the kidneys recruit basophils and activate them to produce interleukin-6 and drive TH17 cell responses.
Around the world, governments are urging populations to receive a third COVID-19 vaccine dose. Here, the authors compare immunogenicity, reactogenicity and effectiveness of a third dose versus the second dose of the BNT162b2 vaccine in a large group of healthcare workers in Israel.
How ILC1s respond to cancer cells is somewhat controversial. Here, the authors show that IFNγ released by ILC1s can control acute myeloid leukemia by promoting leukemia stem cell apoptosis and favoring their differentiation into non-leukemic cells.
To determine how T cell lineage fates are determined in the thymus, Singer and colleagues generated ‘FlipFlop’ mice with a functionally reversed T cell immune system that distinguishes TCR signal strength versus TCR signal duration.
Blander and colleagues show that concurrent detection of LPS and bacterial RNA triggers the interaction of procaspase-11 with NLRP3, upstream of the activation of either receptor and before NLRP3–ASC oligomerization.
Cassatella and colleagues identify CD66b−CD64dimCD115− cells in the human bone marrow as the earliest neutrophil-committed progenitor cells described to date.
How the mitochondrial electron transport chain (ETC) interacts with the NLRP3 inflammasome is somewhat unclear. Here the authors use individual complex inhibitors and new genetic models to show that ETC is critical in providing ATP via the phosphocreatine shuttle to activate the NLRP3 inflammasome.
Perry et al. demonstrate that regulatory T (Treg) cell function is restrained by the cell-autonomous action of the checkpoint inhibitor molecule PD-1. This PD-1-dependent mechanism tunes Treg cell function during homeostasis and infection.
Vignali and colleagues show that the inhibitory receptor LAG3 interferes with TCR signaling and T cell activation by lowering the pH at the immune synapse, which causes the dissociation of the tyrosine kinase Lck from the CD4 or CD8 co-receptor.
Schumacher and colleagues have designed a reporter system that allows in vivo tracking of replicative history over many cell generations. Using this system to study acute T cell responses, they uncover substantial diversity in past division of central memory CD8+ T cells and its link to cell state and recall potential.
Thomas and colleagues describe how multiple SARS-CoV-2 antigen exposures, including mRNA vaccine boosters, primary infection and breakthrough infection, shape T cell immunity.
Tussiwand and colleagues show that an uncommitted precursor expressing the lymphoid-specific factor TdT generates a large fraction of myeloid and a substantial fraction of erythro-megakaryocyte cells.
Nie et al. show that the transcription factor LRF, by upregulating expression of the integrin gene Itgb7, imprints thymic precursors of CD8αα+ intraepithelial lymphocytes for eventual seeding of the gut tissues.
Rinkevich and colleagues show that preexisting matrix is transferred by neutrophils across organs into injured sites in a manner dependent on integrin activation.
Fabry and colleagues show that cribriform plate-resident lymphatic endothelial cells respond to neuroinflammatory signals by inducing functional changes that enhance antigen capture and presentation from the cerebrospinal fluid and promote leukocyte interactions within the central nervous system.
Nahrendorf and colleagues show that B cells in the bone marrow are an important source of the neurotransmitter acetylcholine, which limits hematopoiesis through modulating the signals produced by the bone marrow stromal niche during steady-state and emergency hematopoiesis.