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Amyloid deposits, regardless of clinicopathologic type or tissue involvement, are composed of a loose meshwork of 7.5- to 10-nm fibrils. 1 During the course of purification of extracted amyloid fibril preparations, a further amyloid tissue protein, quite separate from the fibrillar component of amyloid deposits, was identified. 2,3 This novel amyloid tissue protein was termed amyloid P (plasma)-component, or protein AP (AP), because of its antigenic identity to an α-globulin present in the blood of normal individuals. 4–6 AP is a glycoprotein found in tissue deposits of all forms of amyloid in which it has been sought, irrespective of the chemical nature of the amyloid fibril protein, with the single exception of certain intracortical amyloids. 7,8 AP is indistinguishable from, and derived from, the normal plasma glycoprotein serum amyloid P-component (SAP). 7,9,10 A protein which cross-reacts immunochemically with SAP has been shown to be a normal matrix glycoprotein of glomerular basement membrane; we have shown in immunohistochemical studies that this normal tissue form of amyloid P-component (TAP) is also invariably associated with elastic fiber microfibrils in normal, adult, human skin and other tissues. 11,12 This chapter will summarize and review our current knowledge of the biology of amyloid P-component, including its potential role in the maintenance of normal connective-tissue architecture, and the deposition of amyloid deposits.

Contact dermatitis accounts for up to 40% of all occupationally acquired illnesses, with an incidence conservatively estimated at 70,000 new cases per year in the United States, resulting in a cost, in terms of health care and lost productivity, of $22 million annually. If, as suspected, there is gross underrecording of cases, the true cost may lie in the range of $222 million to $1 billion. 1 Atopy is the single greatest risk factor for the development of contact dermatitis; the relative odds of developing occupational skin disease are 13.5 times greater in atopic subjects, 2 who account for 93% of lost jobs, 79% of lost workdays, and 88% of compensation payments. 3 These figures do not, of course, take into account contact dermatitis occurring outside the workplace; up to 3% of the population may be affected by hand eczema alone. 4 The figures also exclude reference to many of the types of plant dermatitis discussed in this issue. Although the majority of contact dermatitis is the result of exposure to irritants, allergic contact dermatitis accounts for a substantial proportion of cases. Despite the clinical importance of allergic contact dermatitis, our knowledge of its pathogenesis—in particular, regarding why a given individual becomes sensitized to a specific contact allergen—remains comparatively restricted. This paper will review what is known about pathologic mechanisms involved in the development of allergic contact dermatitis, incorporating recent information on the immunologie function of normal skin. Recent data on the mechanisms of action of agents that modulate the induction or expression of allergic contact dermatitis, such as topical corticosteroids, mid-range ultraviolet light irradiation (UV-B), and 8-methoxypsoralen plus long-wave ultraviolet light irradiation (PUVA), also will be discussed.