Individuals who are allergic to some things that their skin comes in contact with (a condition called contact dermatitis), such as metals or poison ivy, are treated with glucocorticoids, which can be applied to the skin as a cream or taken orally. Glucocorticoids work by dampening the inflammatory response to the allergen, but precisely which cells they affect and in what way have not been determined for contact dermatitis.
In a recent study in the Journal of Clinical Investigation, Günther Schütz and colleagues from the German Cancer Research Institute, Heidelberg, show that glucocorticoids do not dampen inflammation induced by contact with an allergen in mice lacking expression of the glucocorticoid receptor in immune cells known as macrophages and neutrophils.
Furthermore, for glucocorticoids to dampen inflammation the glucocorticoid receptor had to bind DNA and repress the production of several proinflammatory soluble factors, including IL-1-beta, MIP-2, MCP-1, and IP-10. Conversely, administration of these soluble factors to mice abrogated the protective effects of glucocoticoids following the induction of an allergic response in the skin. The authors therefore suggest that targeting macrophage and neutrophil production of these soluble factors might provide a more specific treatment for individuals with contact dermatitis than glucocorticoids and avoid the side-effects that are associated with long-term administration of glucocorticoids.
Article: Macrophages and neutrophils are the targets for immune suppression by glucocorticoids in contact allergy
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