Volume 16 Issue 7, July 2016

The SOCS family member CIS is a crucial negative regulator of IL-15-induced signalling in NK cells.

Steven Ziegler describes a 1986 study by Mossmannet al. that defined two subsets of T helper cells on the basis of their activities.

Mitochondrial remodelling instructs metabolic adaptations in T cells.

Memory CD4⁺T cells promote vascular permeability, allowing protective antiviral antibodies to access neuronal tissue.

Non-canonical inflammasome activation by self-derived oxidized phospholipid promotes both IL-1β release and cell survival.

Contact hypersensitivity induces a memory NK cell response that requires the NLRP3 inflammasome in tissue-resident macrophages.

Dysregulated inflammasome activation is linked to numerous inflammatory disorders and is therefore tightly regulated. In this Review, the authors discuss the latest insights into the activation and assembly mechanisms of inflammasomes, the structure of distinct inflammasome complexes and the mechanisms that regulate inflammasome signalling.

Structural and functional similarities between the cytolytic synapses formed by CD8⁺T cells and primary cilia are shedding new light on the mechanisms and order of events of synapse formation.

Here, the authors discuss the role of C-type lectin receptor signalling pathways in the control of T helper cell differentiation and examine how these receptors and pathways can be harnessed for vaccine strategies.

A broad and practical overview for applying computational techniques to analyse, visualize and interpret high-dimensional data from flow cytometry. Computational flow cytometry improves reproducibility, allows automated identification of cell populations and biomarkers, as well as enables predictive modelling of clinical correlates and cell development pathways.