Managing Contact Dermatitis

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Science  21 Sep 2007:
Vol. 317, Issue 5845, pp. 1651
DOI: 10.1126/science.317.5845.1651a

Mast cells are traditionally, and perhaps unfairly, associated with the unwanted face of immunity: namely allergies. Yet these cells perform a variety of vital front-line roles, from ejecting worms from the gut, to regulating T cell responses, to protecting us against the toxic effects of animal venoms. Grimbaldeston et al. extend this list of virtues to the attenuation of skin inflammation caused by toxins and ultraviolet (UV) radiation. Mice deficient in mast cells were found to develop a severe form of contact hypersensitivity—similar to the T cell-dependent contact dermatitis seen in humans—after exposure to the hapten dinitrofluorobenzene or to the allergenic plant compound urushiol. Replenishing the mast cell population in these animals with cells cultured from wild-type mice, but not from mice deficient in the immune regulatory cytokine IL-10, was sufficient to significantly reduce the degree of skin inflammation. The ability of mast cells to produce IL-10 depended on engagement of the immunoglobulin Fc γ receptor and corresponded with the suppression of inflammation achieved by administering antigen-specific immunoglobulin. Inflammation caused by UVB irradiation was also dampened by mast cell activities but in this case appeared generally independent of the ability to produce IL-10. These findings may open up new avenues for harnessing the anti-inflammatory power of mast cells to treat inflammatory skin disorders. — SJS

Nat. Immunol. 8, 10.1038/ni1503 (2007).

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