Nature Immunology pp 987 - 994

T cells, a type of immune cell, can impede the development and progression of multiple sclerosis in mice, according to a paper to be published in the September issue of Nature Immunology.

Many different types of T cells exist, each expressing a unique T cell receptor that helps the cell sense and react appropriately to its environment. J. Ludovic Croxford and colleagues show that a specific subset of T cells slows the onset and decreases the severity of a mouse version of human multiple sclerosis. The disease is worsened in the absence of these T cells, which block autoimmunity at least in part by triggering other immune cells to release chemical mediators that dampen the inflammatory response. Whether these T cells are involved in human autoimmune disease, and whether they can be harnessed for therapeutic intervention, remains to be determined.

Nature Immunology pp 971 - 977

A link between zinc and a critical aspect of normal immune cell function is identified by a study to be published in the September issue of Nature Immunology.

Invading pathogens can trigger sensors on immune cells, leading to the expression of proteins important for host defense. Toshio Hirano and colleagues demonstrate that pathogen detection induces changes in the expression of proteins responsible for importing and exporting zinc in immune cells, causing a net depletion of zinc inside cells. Pathogen-triggered zinc depletion inside cells is essential for the upregulation of expression of host defense proteins; immune cells artificially flooded with zinc show blunted pathogen responsiveness. These results suggest that immune cell function hinges on a delicate balance of zinc influx and efflux, and emphasize one specific link between nutrition and immunity.

Nature Immunology pp 929 - 945

A key factor that controls the development of brain inflammation is reported in two studies in the September issue of Nature Immunology. Identification of this factor—called interleukin 27—may provide a new target for treating inflammatory diseases of the central nervous system.

Nico Ghilardi and Christopher A. Hunter and colleagues studied two different mouse models of brain inflammation that resemble human diseases such as multiple sclerosis. Both groups show that brain inflammation is worse in mice that cannot respond to interleukin 27, a factor that communicates messages to immune cells. This more severe brain inflammation is associated with an influx of T cells that produce a molecule known to promote inflammation—interleukin 17—into the brain. The treatment of T cells with interleukin 27 blocks the development of cells that produce interleukin 17. By preventing harmful interleukin 17-producing cells from developing, interleukin 27 could represent a potential therapeutic target for treating autoimmune diseases.