Research Highlights in 2012

Viral infections activate innate immune signalling pathways that impair the clearance of co-infections with bacteria.

Gut pathobionts can trigger sepsis-like disease via the NAIP5–NLRC4 inflammasome.

Surveillance of basic cellular activities alertsCaenorhabditis elegansto pathogens or toxins.

Pro-resolving lipid mediators lower the required antibiotic dose needed to clearE. coliinfection.

Composition of the intestinal flora influences the severity of graft-versus-host disease.

Germinal centre B cells are responsive to BCR stimulation only in the cell cycle G2 phase.

MicroRNA-10a helps to maintain the phenotype of regulatory T cells and prevent conversion to other T cell fates.

Adaptor protein 3 delivers TLR4 to phagosomes for pro-inflammatory signalling and effective MHC class II-mediated presentation of phagocytosed antigens.

Immunostimulatory conventional dendritic cells can differentiate into immunosuppressive macrophage-like cells.

Inflammasome activation has a protective effect in age-related macular degeneration.

Oral treatment withLactococcus lactismodified to secrete pro-insulin and IL-10, when combined with systemic low-dose CD3-specific antibodies, reverses diabetes in NOD mice.

Actin filaments exposed by dying cells are a damage-associated molecular pattern sensed by dendritic cells.

Most tissue macrophages in mice are derived from the yolk sac and not from haematopoietic stem cells.

The development of medullary thymic epithelial cells and γδ T cells is linked through RANK signalling.

Three papers describe mechanistic links between commensal bacteria and immune disease susceptibility.

Innate functions of B cells are important for antiviral immunity.

A new MRI technique can accurately predict diabetes development in NOD mice.

Two studies uncover details of the antigens and immune responses that are involved in cancer immunoediting.

Skin-resident effector memory CD8⁺T cells provide long-lasting immune protection in the skin.

Activating stimuli identified for the NLRP3 and NLRP7 inflammasomes.