Articles in 2015

Signalling by pattern-recognition receptors (PRRs) is finely tuned by many regulators and amplifiers, and a complex interplay between PRR pathways and other immune receptor pathways helps to ensure that appropriate immune defence pathways are initiated and coordinated. Xuetao Cao describes some of the latest advances in this complex regulation.

In this Review, the authors relate the growing appreciation of the neuroimmune circuits that link inflammatory and immune responses with depressive behaviours. They explore the evolutionary basis of this neuroimmune link and discuss how a better understanding of these pathways may lead to new therapies that treat depression by targeting the immune system.

Single-cell RNA sequencing identifies T helper 17 cell heterogeneity and regulators of pathogenicity.

Here, the authors detail our current understanding of specialized pro-resolving mediators (SPMs), a family of endogenous mediators that have important roles in promoting the resolution of inflammation. With a focus on the lungs, they discuss the contribution of SPMs to infectious and chronic inflammatory diseases and their emerging therapeutic potential.

In this Review, the authors detail the emerging evidence that supports the existence of memory populations of regulatory T (T_Reg) cells. They explain the immunological settings in which memory T_Regcells develop, discuss the physiological relevance of these cells and address some of the key questions that remain for this rapidly evolving field.

The recent discovery that some memory T cells can become tissue resident after infection warrants further study into the mechanisms and therapeutic implications of such enhanced regional immunity.

An intronic element ofFoxp3 facilitates the selection of T_Regcells with a diverse TCR repertoire for effective self-tolerance.

T cell receptor-stimulated regulatory T cells cluster with self-reactive T cells to receive signals from interleukin-2 and maintain immune homeostasis.

Two papers inSciencepresent evidence in mice that certain species of intestinal bacteria can drive antitumour immune responses and modulate responses to immune checkpoint blockade.

An early innate immune response is induced at the epithelium during viral infections, independently of interferons.

Accumulating data are highlighting new roles for the caspase family of cysteine proteases beyond their well-established functions in apoptosis and inflammation. This Review describes these emerging roles for caspases in mediating distinct forms of programmed cell death and directing inflammasome and innate immune responses.

Tolerance to commensal skin microorganisms relies on early bacterial colonization and an influx of regulatory T cells into neonatal skin.

SOCS family member CISH hushes T cell receptor signalling and limits tumour killing.

Activation of STING (stimulator of interferon genes) by cytosolic aberrant DNA species or cyclic dinucleotides triggers transcription of numerous innate immune genes. In this Review, the author summarizes recent insights into the regulation of STING signalling and its role in autoinflammatory disease and cancer.

This Review describes the role of the immune system in dengue pathogenesis. The authors also discuss new insights gained from human monoclonal antibodies against dengue virus as well as the recent vaccine trials and the challenges to develop an effective dengue vaccine.

Macrophages populate the body's tissues and organs, where they become highly specialized to preserve organ integrity in the event of microbial invasion or injury. A dynamic crosstalk between the macrophages and their surrounding tissue cells is crucial to ensuring this homeostatic function. This Review highlights the key molecules and mechanisms involved in macrophage–tissue interactions.

Sarah Gaffen describes a 2006 paper by Toyet al. that elucidated the subunit composition of the receptor for IL-17.

Oestrogen receptor-β promotes immune evasion of endometriotic tissue by blocking TNF-induced apoptosis and enhancing inflammasome activity.

This Opinion article proposes that interleukin-15 (IL-15) is a master regulator of tissue-specific T cell responses to promote the destruction of infected cells. Hence, dysregulation of IL-15 production in tissues during sterile inflammation can lead to T cell-mediated autoimmunity.

Researchers design switchable therapeutic T cells that can be remotely activated by a small-molecule drug.