Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
In this Viewpoint article, Nature Reviews Immunology invites 18 experts to discuss the nature of T cell exhaustion. How should T cell exhaustion be defined and what are the developmental relationships between exhausted T cell subsets? The contributors share their thoughts on key recent developments in the field.
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.
Two papers by Gregory Barton and colleagues identify distinct UNC93B1-dependent mechanisms for regulation of the endosomal nucleic acid-sensing TLRs, TLR7 and TLR9.
Host-derived molecules, the so-called damage-associated molecular patterns (DAMPs), can induce sterile inflammation. This Review provides an overview of DAMP-sensing receptors, discusses the crosstalk between these receptors and explores their role in disease.
Chimeric antigen receptor (CAR) T cells directed at fibroblast activation protein show efficacy in mouse models of hypertensive cardiac injury and fibrosis.
Commensal bacteria at mucosal surfaces can remotely control the thymic maturation of mucosal-associated invariant T cells through the production of microbial factors that enter the circulation and are taken up by thymic cells.
The authors consider the inflammatory basis of type 1 and type 2 diabetes. In particular, they focus on the role of IL-1β in both diseases and discuss the feasibility of targeting innate immune mechanisms in the clinic.
A new study shows that monocytes, recruited to the lungs during an infection, sense alterations in physical forces and pressure and initiate a pro-inflammatory response. This environmental sensory axis is mediated by the mechanically activated calcium channel PIEZO1.
Prue Hart describes a 1983 paper by De Fabo and Noonan that identified urocanic acid as a major photoreceptor for ultraviolet radiation in the skin that induces systemic immunosuppression.
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.
Recent advances in single-cell antibody cloning technologies have enabled the molecular characterization of monoclonal antibodies against Plasmodium falciparum parasites, which has significantly enhanced our understanding of how these antibodies are generated, as well as their epitope specificity and binding modes.
The angiogenic growth factor placental growth factor is produced by TH17 cells and induces TH17 cell differentiation, which suggests a positive feedback loop between angiogenesis and autoimmunity in chronically inflamed tissues.
Class-switch recombination was thought to take place in B cells that enter germinal centres, but this study shows that it actually occurs earlier than previously thought.
Universal cells — here defined as cells that are invisible to the immune system — could potentially have many uses in transplantation medicine. This Review discusses how far we have come in creating such cells and the lessons that nature can teach us about immune evasion.
Platelets are best known for their roles in haemostasis, but they also contribute to host immunity. In this Review, Gaertner and Massberg consider how platelets ‘patrol the vascular highway’ to shape immune responses during infection and cancer.
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.
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.
