Volume 14 Issue 9, September 2014

Linear ubiquitylation of the adaptor protein ASC regulates interleukin-1β production by the NLRP3 inflammasome.

Regulatory T cells suppress effector T cells by releasing exosomes that contain microRNAs.

Eosinophils initiate T helper 2 cell responses in the small intestine by promoting dendritic cell activation.

Pulmonary epithelial cells drive rhythmic neutrophil recruitment by secreting chemokines in a clock-dependent manner.

NOD2 restricts small intestinal inflammation by controlling the overgrowth of commensal bacteria.

A new study identifies inflammatory caspases as the cytoplasmic LPS receptors that trigger non-canonical inflammasome activation.

T helper 17 (T_H17) cells promote protective immune responses against infection, particularly at barrier sites, but they can also have pathogenic roles in inflammatory diseases. In this Review, the authors describe the factors that control the development and maintenance of T_H17 cells, and discuss their diverse functions in both health and disease.

There is a growing appreciation of how the host inflammatory response is intricately entwined with the various forms of programmed cell death. This Review discusses the signalling mechanisms that link these processes, with a particular focus on how the key mediators of cell death, such as the caspases, are integrated into innate signalling modules.

There is currently no single model that fits the wealth of experimental data that relate T cell activation to T cell receptor–peptide–MHC binding parameters. Here, the authors analyse and reformulate the published models, and suggest that a kinetic proofreading model that involves limited T cell receptor signalling provides the best fit.

Recent evidence indicates that adaptive T cell-mediated immune responses can regulate innate lymphocytes (natural killer cells and innate lymphoid cells) in an interleukin-2-dependent manner. The authors propose a model in which adaptive T cells function as peripheral antigen-specific sensors that recruit and activate innate lymphocytes to amplify and coordinate local immune responses.

Natural killer T (NKT) cell defects have been implicated in several diseases such as autoimmunity, asthma and cancer, but will targeting them really be of clinical benefit? Here, the authors investigate this question and conclude that more careful studies are needed before the true clinical potential of NKT cell-targeted therapies can be determined.