IMMUNOLOGY : Stop that itch!
Immune cells in the skin secrete a chemical that limits the inflammatory response to poison ivy and sunburn.

Stephen Galli and colleagues look at how the immune system responds to irritants such poison ivy and poison oak or to sunburn, all of which can lead to blistering of the skin. Their research identifies mast cells, a form of immune cell that resides in the skin, as the source of interleukin 10 (IL-10), a molecule known to suppress immune responses. Mice that lack mast cells or have mutant mast cells that are unable to make IL-10 develop larger skin lesions, which last much longer, than those of normal mice upon exposure to the irritant found in poisonous plants. The mutant mice also display higher numbers of T cells recruited to the affected skin lesions.

The work identifies a new role for mast cells, which have been previously associated with releasing mediators of allergic reactions. The authors utilize these findings to manipulate mast cell release of IL-10 in settings of skin inflammation and irritation to limit further damage. These findings might lead to new therapies for skin damage.


Author contact:
Stephen Galli (Stanford University School of Medicine, Stanford, CA, USA)
Tel: +1 650 723 7975; E-mail: sgalli@Stanford.edu


Restraining allergic responses


A cellular process crucial for preventing allergy.
Certain varieties of immune cells release interleukin 4, a protein that, upon binding to its receptor, triggers signals that promote hallmark features of allergy. Yoshinori Fukui and colleagues show that interleukin 4 receptors expressed on the surface of immune cells called T cells are quickly internalized, directed along the complex network of protein ‘fibres’ that support T cell structure and shape, and ultimately routed into cellular compartments for degradation. This ‘harness’ on interleukin 4 expression is interrupted in T cells lacking Dock2, a protein responsible for regulating the ‘trafficking’ of internalized cargo. As a result Dock2-deficient T cells display excessive amounts of interleukin-4 receptors and Dock2-deficient mice suffer from spontaneous allergic inflammation. Whether Dock2 regulates the intracellular fate of other T cell surface proteins remains for future investigations.

Author contact:

Yoshinori Fukui (Kyushu University, Fukuoka, Japan)
Tel: +81 92 642 6828; E-mail: fukui@bioreg.kyushu-u.ac.jp