Research Highlights in 2016

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

Maternally derived commensal-specific IgG helps to limit mucosal T cell responses in neonates.

Mice lacking CARD9 have altered microbiota with impaired tryptophan metabolism and therefore increased susceptibility to colitis.

HOBIT and BLIMP1 identified as universal regulators of tissue residency in lymphocytes.

The innate immune receptor LILRA2 (leukocyte immunoglobulin-like receptor subfamily A member 2) senses microbially cleaved immunoglobulin.

The Fanconi anaemia DNA repair pathway also has cytoplasmic functions in selective autophagy that might contribute to an inflammatory pathology of Fanconi anaemia disease.

Exposing mice to a dirty environment helps to 'humanize' their immune system.

Asymmetric distribution of metabolic pathway components sustains differential CD8⁺T cell fates.

Cyclodextrin promotes atherosclerosis regression through oxysterol-mediated, LXR-dependent macrophage reprogramming.

Biological scaffolds create an immune microenvironment that is favourable for tissue regeneration.

Circulating tumour cells fragment as they metastasize, providing 'information' to immune cells that promote or inhibit metastasis.

Peritoneal cavity macrophages are rapidly recruited by a non-vascular route to the injured liver to mediate tissue repair.

Arginase 1 regulates ILC2 metabolism and the development of type 2 inflammation in the lungs.

Autophagy regulates survival and lineage stability in peripheral regulatory T cells.

Maternal immune activation can lead to autism-like behaviour in offspring, and in mice this depends on maternal interleukin-17A production.

Ageing muscles fail to accumulate regeneration-promoting regulatory T cells after injury.

Nuclear factor-κB signalling induces p62-dependent autophagy of damaged mitochondria to limit NLRP3 inflammasome activation.

The release of sphingosine-1-phosphate from dying cells activates erythropoietin signalling in macrophages, which enables immunologically silent clearance of dying cells.

Weaning onto solid food induces regulatory T cell populations in the small intestine that help protect against food allergy.