Cytokines and Langerhans cells in allergic contact dermatitis.

Contact hypersensitivity (CHS) is a dendritic cell (DC)-dependent T-cell mediated cutaneous inflammatory reaction elicited by epicutaneous exposure to reactive chemicals, known as haptens, from cosmetic products or through environmental and occupational exposures. The best-studied haptens are low molecular weight chemicals (<1,000) that bind discrete amino acid residues on self or exogenous proteins/peptides in the skin and become immunogenic. Clinically, CHS typically occurs as a delayed type of allergic contact dermatitis. Haptens penetrate the skin and bind to self proteins to form complete antigens which are taken by antigen presenting cells to start a cascade of actions resulting in a delayed hypersensitivity reaction. Larger molecules such as proteins induce response involving the humoral immune system. The environment at the time of antigen presentation affects the innate immune system which in turn influences the expression of CHS. The subsequent immunologic response (or lack thereof) is a result of complex interaction between both the innate and the adaptive immune systems. This interaction results in either an inflammatory immune response or tolerance.