Volume 17 Issue 3, March 2017

During systemic infection interleukin-22 can limit the availability of iron by promoting increased production of haem scavengers.

Pseudogenization of a singleSalmonellaeffector protein gene facilitates pathogen hijacking of dendritic cells to spread systemically.

CYP1 enzymes expressed by intestinal epithelial cells metabolise AHR ligands in the gut to regulate intestinal immune responses.

MTORC1-dependent macrophage proliferation and glycolysis drive granuloma formation in sarcoidosis.

Michael McHeyzer-Williams describes a 1998 study by Avi Kupfer and colleagues that transformed the view of cognate T helper cell–B cell crosstalk.

This Review describes how different modes of cell death protect against bacterial and viral infections, and the complex signalling crosstalk between the different pathways during an infection.

Following muscle injury, changes in the stages of muscle growth coincide with changes in the phenotype and activation status of leukocytes that enter the site of muscle damage. As described in this Review, complex and coordinated crosstalk between immune cells and muscle cells determines the success or failure of muscle regeneration.

This Review focuses on the protective and pathological roles of different T cell subsets in the central nervous system (CNS). The authors explain how effector, memory and regulatory T cell populations are primed and recruited to the CNS, and discuss the plasticity of these populations, particularly in the context of viral infection and autoimmunity.

Severe haemorrhagic fever is a feature of infection with both Ebola and Lassa viruses, but differences in the immune responses induced by infection in each case may have important implications for the development of specific therapies and vaccines.

Innate immune responses are triggered in response to the sensing of pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs) by pattern recognition receptors (PRRs). An emerging idea is that inflammasome activation may also occur independently of PRR activation following a disturbance in cellular homeostasis. The authors explore this concept and the implications for chronic inflammatory disease in this Opinion article.