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Dietary long-chain fatty acids enhance the differentiation of TH1 and TH17 cells in the gut, which worsens disease in a mouse model of multiple sclerosis.
The kinases MST1 and MST2, which are activated by Toll-like receptor stimulation, regulate the trafficking of mitochondria to phagosomes to deliver reactive oxygen species.
This Essay considers how prokaryotic and mammalian immune systems ensure tolerance or resistance to genetic elements. In particular, the authors discuss the restriction–modification and CRISPR–Cas activities of prokaryotes and the analogous immune pathways found in mammals.
Emerging evidence suggests that the stroma of the tumour microenvironment can shape antitumour immunity and responsiveness to immunotherapy. The stromal cells and the signals they produce that influence tumour-infiltrating leukocytes, as well as the implications for cancer treatment, are reviewed here.
Reciprocal interactions between leukocytes and endothelial cells enable leukocytes to recognize the blood vessel endothelium in areas of inflammation and transmigrate across the endothelial barrier to mount an immune response in infected and/or damaged tissues.
Here, the authors explain how the specificity and magnitude of the primary cytotoxic T lymphocyte (CTL) response is determined during a viral infection. They discuss the different factors that influence the recruitment and expansion of naive CTL precursors, and they explain how technological advances have enabled a more accurate quantitation of these responses.
γδ T cells have unique specificities, high clonal frequencies and a pre-activated differentiation status that allow rapid and non-redundant responses to tumours. Here, the authors review their often contrasting roles in cancer and the opportunities for γδ T cell-based cancer therapies.
The rapid response of innate immune cells requires metabolic reprogramming to support their specific effector functions. As discussed here, mTOR is a key regulator of this process: it senses the environmental and intracellular nutritional status of innate immune cells to dictate and optimize the inflammatory response.