A video describing the mechanism of action for poison ivy and other plants containing<unk> .<unk>  is fat-soluble, penetrating the stratum corneum of the skin, then binding to Langerhans cells in the epidermis. The affected cells then migrate to lymph nodes, where T cells become activated, then return to the skin where they stimulate an<unk> -activated dermatitis. The toxic effect is indirect, mediated by an<unk>  immune response. The oxidized<unk> s act as haptens, chemically reacting with, binding to, and changing the shape of integral membrane proteins on exposed skin cells.<unk> s are oxidized in vivo, generating a quinone form of the molecules. Affected proteins interfere with immune system ability to recognize these cells as normal parts of the body, causing a T-cell-mediated immune response. This response is directed at the complex of<unk>  derivatives (namely, pentadecacatechol) bound in the skin proteins, attacking the cells as if they were foreign bodies.
Urushiol-induced contact dermatitis
Phototoxic tar dermatitis
Allergic contact dermatitis
Blister beetle dermatitis
Autosensitization dermatitis
Rodent mite dermatitis
Contact dermatitis
Irritant contact dermatitis