Pathogenesis of contact allergic dermatitis

In the afferent phase of ACD, a naïve host is exposed (over time) to a low molecular weight hapten, which chemically reacts with epidermal proteins. These epidermal proteins are taken up by cutaneous antigen presenting cells (Langerhans cells and other APC), and trafficked to the local lymph node where education of conventional T-cells occurs. This results in the development of T memory/effector lymphocytes. At the same time during the afferent phase of ACD, innate immunity is also activated. Epidermal glycolipids are released, and presented to invariant NKT-cells, which interact with CD1d bearing B-cells, which produce hapten specific IgM. During the efferent phase, upon re-exposure to the hapten, memory T-cells are mobilized to the site of hapten challenge by hapten specific IgM which fixes complement, and activates endothelial cells, promoting conventional T-lymphocyte trafficking into the challenge site. CD8+ T-lymphocytes, along with innate immune cells such as NK- and NKT-cells, are thought to be effector cells of ACD. This group of cells releases cytokines and mediates cytotoxicity to APC and epidermal KC, resulting in the clinical signs and symptoms of ACD.