Volume 20 Issue 1, January 2020

The benefits of exercise reach the bone marrow, altering haematopoietic cell niches and regulating inflammatory cell output.

Activated CD8⁺ T cells adapt to glutamine blockade through upregulation of acetate metabolism, whereas cancer cells lack this flexibility and are highly susceptible to glutamine blockade.

Ana Domingos describes a 1994 paper by Jeffrey Friedman and colleagues that identified the hormone leptin as the key regulator of body fat.

Chen Dong and colleagues describe a positive-feedback loop between TOX2 and BCL-6 that helps to drive the development of T follicular helper cells in germinal centres.

A trispecific antibody that provides T cell co-stimulation shows promise in preclinical models of myeloma.

Stress-induced metabolic changes in CD4⁺ T cells linked to anxiety-type behaviours.

There is growing interest in harnessing dendritic cells for cancer immunotherapy. Here the authors describe the roles of dendritic cells in the tumour microenvironment and the different strategies that are being developed to target these cells in the clinic.

Understanding why some patients and not others respond to immune checkpoint blockade for cancer is crucial for extending benefit from this therapy. Here the authors describe how tumour cells can resist immune checkpoint blockade, for example, by resistance to interferon signalling and through immune-evasive oncogenic signalling pathways.

Here, the authors describe how metabolic disorders, such as type 2 diabetes and nonalcoholic fatty liver disease, are driven by alterations in the composition of the intestinal microbiota and its metabolites, which translocate from the gut across a disrupted intestinal barrier and contribute to metabolic inflammation.

Emerging studies highlight cell metabolism as a crucial regulator of T cell quiescence and activation. This Review describes how immunological cues and nutrients fine-tune metabolic programmes and signalling networks that together promote T cell quiescence exit.