We investigate skin disease, skin and cardiac allograft rejection, and T cell recruitment to inflammation in peripheral tissues.
Epidermal application of reactive haptens such as urushiol, the reactive agent in poison ivy, and subsequent challenge results in the development of a T cell mediated inflammatory response termed allergic contact dermatitis or contact hypersensitivity (CHS). Using several different strategies we have observed that hapten application primes two reactive T cell populations: IFN-g producing CD8+ T cells which are the effector T cells of the response and CD4+ T cells producing IL-4, IL-5 and IL-10 which regulate the magnitude and duration of the CHS response. Once primed, recruitment of the CD4+ and CD8+ T cells to tissue challenge sites requires a complex cascade of chemokine production and leukocyte infiltration. This cascade is initiated when hapten induces keratinocytes to produce chemoattractants such as Groa which recruit neutrophils to the challenge site. The goal of our studies is to define the neutrophil derived products and/or activities which lead to the recruitment of the hapten-primed T cells to the site and the effector functions expressed by the T cells following activation by the hapten at the site to elicit the CHS response.