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Tanaka and colleagues show that an SNX25–Nrf2 pathway in dermal macrophages sets the threshold for pain sensitivity through modulating the production of the neurotrophic factor NGF.
Caligiuri and colleagues show that the m6A reader YTHDF2 modulates the inflammatory activation and antitumor function of tumor-associated macrophages in part by modulating the stability of Stat1 mRNA.
Colonna and colleagues report dysregulated gene expression in microglia harboring homozygous mutations of DAP12 from individuals with Nasu–Hakola disease, a form of early-onset dementia.
Reboldi and colleagues show that high-cholesterol diets influence IgA secretion. Cholesterol-derived metabolites act on plasma cell GPR183 receptors to alter cell positioning of IgA+ plasma cells within the lamina propria and suppress antibody responses to intestinal pathogens.
Farber and colleagues examine the phenotypic, transcriptomic, clonal, and functional differences between tissue-resident T cells in various barrier tissue sites relative to T cells in lymphoid organs and circulation in humans.
The formation of an immunological synapse is central to the ability of NK cells to lyse target cells. Here the authors show that Nogo receptor 1 (NgR1) might be a good target for cancer immunotherapy as it destabilizes the NK synapse, resulting in defective killing of tumor cells.
Here, the authors show that a subset of NKT2 cells are programmed during thymic development at early postnatal ages to migrate to the skin, where they support local tissue homeostasis through regulation of iron metabolism.
Trained immunity can manifest as a form of innate immune memory whereby innate immune cell responses are reprogrammed to respond differently to a variety of stimuli. Here, the authors show that lung macrophages can be trained by whole beta-glucan particle to enhance their ability to control tumor metastasis.
Gasdermin E pore formation has been associated with pyroptotic cell death. Here the authors identify gasdermin E pores in a subset of human TH17 cells and show that rather than killing these cells the pores enable the release of IL-1α on NLRP3 inflammasome activation as an antifungal immune response.