Harmful effects produced by the mechanisms of cell-mediated immunity are referred to as delayed hypersensitivity.
Delayed hypersensitivity is mediated by Th1 cells, also called TD cells, and is responsible for contact dermatitis, tissue damage in a variety of infectious disease, and rejection of tissue grafts.
A contact hypersensitivity such as poison oak dermatitis is initiated be contact with the antigen, which is also called the allergen.
During contact, a small molecule from the plant, called a hapten, binds to carrier protein in the host.
The carrier protein with bound hapten is ingested by a macrophage and the hapten-peptide is then presented on the surface of the macrophage on a Class II MHC.
Th1 cells with T-cell receptors capable of recognizing the hapten-peptide antigen interact with the presented antigen, become activated and increase in numbers.
When the host comes in contact with the allergen a second time, the Th1 cells react with the hapten-peptide being presented on the macrophage and release cytokines resulting in attraction of more macrophages, followed by inflammation and skin lesions.
Characteristic skin lesions appear after 24 hours, reaching their peak at 48-72 hours after this second exposure to the plant.