Allergic contact dermatitis to poison ivy (Toxicodendron radicans) is believed to be mediated by T lymphocytes specific for the
hapten urushiol. Activated T lymphocytes may produce pathology by a variety of mechanisms including direct cytotoxicity, production of
lymphokines, recruitment of non-specific effector cells, non-specific cytotoxicity, and possibly autologous DR reactivity. The regulation and pathogenesis of this condition was studied by cloning and characterizing
urushiol-specific T cells from the peripheral blood of patients with
poison ivy dermatitis. Multiple CD8+ (T8+)
urushiol-specific clones were derived. All clones that proliferated in response to a
crude extract of T. radicans also proliferated in response to purified
urushiol. Thus,
urushiol appears to be the single immunogenic component of T. radicans resin. Pentadecylcatechol (PDC), which differs from
urushiol only in the lack of unsaturated bonds in its lipophilic tail, stimulated only one of seven clones tested. This suggests that the double bonds in the C15 lipophilic tail of
urushiol are required for antigenicity. Several of the CD8+
urushiol-specific clone suppressed
pokeweed mitogen-induced
IgG production in the presence of
urushiol. Suppression was triggered specifically by
urushiol and required MHC compatibility both for the antigen-presenting cells and the responding B cells. These suppressor clones were isolated from convalescent blood and may represent a mechanism for the termination of an
allergic contact dermatitis.