Mast cells are involved in a multitude of biological functions but are probably best known for their role in IgE-mediated Type 1 hypersensitivities. In the skin, mast cells play a critical role in regulating homeostasis and provide protection from the inflammatory effects of exposure to contact allergens and ultraviolet (UV) radiation. The release of histamine and neuropeptides from dermal mast cells following exposure to environmental insults like UV may explain the itching response (pruritus) that is induced by sunlight. This implies that mast cell-derived inflammatory mediators may promote pruritus in UV-exposed skin. Contrary to this prediction, we have discovered that mice deficient in mast cells are highly sensitive to UV-induced pruritus. We used a chronic UV irradiation regime consisting of two sub-inflammatory UV(B) exposures per week given over 4 weeks. This protocol is similar to that administered for prophylaxis in certain photodermatoses in humans. Compared to controls, UV-exposed mast cell-deficient KitW-Sh/W-Sh mice were more susceptible to dermal oedema which was linked to blood vessel dilation. Furthermore, KitW-Sh/W-Sh mice were resistant to phototolerance induction (as measured by an increase in skin swelling and epidermal thickening) by photohardening treatment. To our surprise, these mice also exhibited an excessive scratching behavior following broad band UVB plus UVA or solar simulated UV irradiation at doses far below their minimal skin swelling dose. Protection from this UV-induced scratching phenotype was dependent on mast cells, since engraftment of KitW-Sh/W-Sh mice with bone marrow derived-cultured mast cells abated it entirely. While it is well known that mast cells are required for UV-induced immune suppression, we have discovered that they protect from UV-induced skin oedema and itching.