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The mechanisms underlying immediate contact skin reactions are only partially understood, especially regarding nonimmunologic contact urticaria (CoU) and protein contact dermatitis (PCD). Each trigger substance has its own mechanism or mechanisms of action. Nonimmunologic CoU is due to vasogenic mediators without the involvement of immunological processes. The pathogenesis of immunological CoU reflects a type I hypersensitivity reaction, mediated by allergen- specific immunoglobin E (IgE) in a previously sensitized individual. Skin challenge involves allergen penetration through the epidermis, IgE binding on mast cells (MCs), their degranulation, and subsequent release of histamine and other vasoactive substances such as prostaglandins, leukotrienes, and kinins (Figure 4.1).A combination of type I and type IV allergic skin reactions, the latter supported by positive delayed patch tests, has been suggested as PCD pathogenesis. It has been speculated that PCD is an eczematous IgE-mediated reaction through proteins. PCD shows a similar reaction pattern to aeroallergen-induced atopic eczema or dermatitis.In this chapter, we will focus on the characteristics involved in immunological immediate skin reactions, especially in CoU. The mast cell’s role is thoroughly discussed.