Allergic contact dermatitis is induced by a wide variety of drugs that trig
ger specific immune responses following topical exposure. Identified chemic
al stuctures involved in such reactions include the mercuric and thiosalicy
lic acid groups of thimerosal, the diphenylketone group of the anti-inflamm
atory drug ketoprofen, the amide or ester structure of local anesthetics, a
nd the sidechain and thiazolidine ring of beta-lactams. The T cell response
s to such compounds involve CD4(+) and CD8(+) alpha beta(+) T lymphocytes a
nd also CD4(-)/CD8(-) gamma delta(+) T cells. Although "T helper" cytokine
production by drug-specific human T cells from patients with allergic conta
ct dermatitis has been described, T helper 1-like and T cytotoxic 1-like re
sponses clearly play key roles in this cutaneous reaction.