Volume 12 Issue 2, February 2012

Intraendothelial chemokine-containing vesicles promote transendothelial T cell migration.

IgA⁺plasma cells in the gut acquire novel effector mechanisms to maintain homeostasis.

Developing T_H1 cells pass through a transitional T_H1–T_FHcell stage.

Loss of TRAF1 expression associates with T cell dysfunction in chronic infection.

A potential new strategy to improve the therapeutic efficacy of targeting the type I IFN pathway in multiple sclerosis.

IL-15 increases mitochondrial biogenesis and spare respiratory capacity in memory T cells.

Programmed cell death of infected host cells builds up the first line of defence against viruses. Here, Mocarski and colleagues describe the tight regulation of caspase 8-dependent apoptosis and programmed necrosis and discuss how viral inhibitors of cell death may have contributed to the evolution of programmed necrosis to promote host survival.

This Review article looks at how the features of vertebrate adaptive immunity — specificity, self-tolerance and memory — can be achieved in plants through different immune strategies.

The dendritic cell (DC) network consists of several DC subsets with distinct functions. Here, Gabrielle Belz and Stephen Nutt focus on transcription factors that regulate DC lineage specification in response to developmental and environmental cues.

Allergic contact dermatitis is a common skin disease that is driven by an inappropriate immune response to innocuous environmental antigens. This Review focuses on how the early immune mechanisms that are triggered in response to contact allergens promote subsequent disease development.

Type I interferons (IFNs) have become synonymous with antiviral immunity. But, as discussed in this Review, type I IFNs also have roles in bacterial infections, in intestinal homeostasis and in inflammatory and autoimmune diseases.

Immunity to viruses is typically associated with the development of cytotoxic CD8⁺ T cells. However, CD4⁺ T cells are also important for protection during viral infection. Here, the authors describe the various ways in which different CD4⁺T cell subsets can contribute to the antiviral immune response.