Contact Dermatitis

Abstract

Chemicals that induce contact sensitivity (CS), called haptens, exhibit several common features that define them as allergens. They are of relatively low molecular weight and are chemically reactive and lipid soluble. In most cases, chemical reactivity leads to the formation of nonreversible chemical bonds between haptens and the cell surface and/or extracellular matrix proteins. This modification of self-proteins has been given several names, such as derivatization, haptenization, and conjugation. By binding to formerly nonimmunologic self-proteins, haptens convert them into immunogenically altered self-proteins recognized by antigen-specific T cells. Conjugates of protein and hapten become the target structures against which contact hypersensitivity (CH) responses are directed. The lipid solubility and small molecular weight allow these chemicals to easily enter the skin through the stratum corneum. Whereas some haptens induce sensitization in humans or animals, others, although of very similar structure, cause irritation or even tolerance induction. In contrast to haptens, substances such as sodium lauryl sulfate or sodium dodecyl sulfate cause rather nonspecific dermatitis and are called irritants. The mechanism by which allergic and irritant contact dermatitis are induced and the differences between these two immune reactions have been of long-standing interest for scientists. As early as 1942, Landsteiner and Chase [1] successfully showed that cutaneous reactivity against allergens could be conferred on immunologically naive guinea pigs by the adoptive transfer of peritoneal exudate from sensitized donors. These experiments for the first time established the transferability of CH with cells.