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In humans and mice, chronic UVB irradiation (wavelengths; 290–320 nm) induces cutaneous inflammation, photoaging, and gene mutations that can lead to the development of malignan-cies at affected sites (Kligman, 1996; Melnikova and Ananthaswamy, 2005). Although factors that promote UV-induced innate responses have been investigated intensively (Melnikova and Ananthaswamy, 2005), less is known about regulatory mechanisms that can limit UVB-induced inflammation. Although mast cells were once thought to function primarily as proinflammatory effector cells that can contribute to either allergic reac-tions (Galli et al., 2005) or inflammation caused by innate responses to exogenous environmen-tal agents such as UV irradiation (Metz et al., 2006), recent evidence indicates that, in certain settings, mast cells can also limit inflammation and tissue injury, including that induced by UVB irradiation (Grimbaldeston et al., 2007; Galli et al., 2008). Mast cells are well positioned to participate in cutaneous immune responses, as skin mast cells are located predominately in the dermis near blood and lymphatic vessels and nerves. Although the majority of UVB rays do not penetrate to the dermis (Noonan and De Fabo, 1992), the UVB-dependent activa-tion of dermal mast cells is thought to be achieved indirectly, e.g., via nerve growth fac-tor derived from the epidermis (Hart et al., 2002; Townley et al., 2002) or by sensory C fi-bers (which innervate the epidermis and ex-tend into the dermis) that have been activated by cis-urocanic acid (Hart et al., 1999, 2002; Khalil et al., 2001). Such indirect mechanisms of mast cell activation contribute to the UVB-induced systemic immunosuppression of acquire