Volume 15 Issue 6, June 2015

A newly discovered B cell-derived peptide inhibits T cell migration during inflammatory responses.

Tumour-associated eosinophils support CD8⁺T cell-mediated rejection through chemoattraction and vascular normalization.

T helper 17 (T_H17) cells transdifferentiate into T regulatory type 1 (T_R1) cells and contribute to the resolution of inflammation in mice.

A newly identified protein, LEM, promotes CD8⁺T cell proliferation and memory formation.

This Review considers the impact of host temperature on the immune system. In particular, the authors focus on how the thermal element of the fever response can shape both innate and adaptive immune responses.

Fibroblastic reticular cells — which are immunologically specialized myofibroblasts of mesenchymal origin — create a network within lymph nodes that is essential for immunological health through interactions with B cells, T cells, dendritic cells and high endothelial venules.

In this Review, the authors describe how tumour necrosis factor (TNF) signals via its receptors. They explain how TNF is able to promote cell survival or cell death in different contexts and discuss the consequences of deregulated TNF receptor signalling for chronic human diseases. Finally, they discuss new strategies for targeting TNF in the clinic.

Outer membrane vesicles (OMVs) are produced by bacteria and can interact with leukocytes and other host cells to shape the immune response during infection. OMVs can have both pro-inflammatory and anti-inflammatory effects; in this Review, the authors discuss how they may contribute to human diseases and also their potential as vaccine adjuvants.

Cytotoxic lymphocytes recognize virus-infected and transformed cells and kill them by apoptosis. Recent studies on the structural and cellular biology of the key mediators of this cytotoxicity — perforin and granzymes — have advanced our understanding of their mechanisms of action, their regulation and the pathophysiological consequences of impaired cytotoxicity.