Good news is on the way for the unlucky ones who've suffered from an itchy rash after an encounter with poison ivy. Researchers have made significant progress in discovering the underlying mechanisms that mediate the reaction to irritant agents such as poison ivy. In fact, poison ivy is one of many agents that produce a response that falls under the classification of allergic contact dermatitis (ACD), or contact hypersensitivity (CHS). However, to truly appreciate this relevant research it's important to understand a bit about CHS.
CHS is essentially a hypersensitive immune response to reactive molecules that bind to your skin (1). All immune hypersensitivities (not just CHS) occur in two phases. In the primary phase, the sensitization stage, a normal primary immune response is mounted to a pathogen. The effector stage consists of a hypersensitive or excessive response to that same pathogen upon subsequent exposure (1). These pathogens can be therefore be referred to as allergens. This type of allergic reaction is mediated by T cells (a type of white blood cell that helps defend against pathogens) and can be caused by a variety of molecules. However, it's important to note that dendritic cell (DC) activation must occur before a T cell response can be mounted. DCs are the immune cells that absorb invading pathogens and subsequently present proteins derived from that pathogen to other immune cells, such as T cells, so that an immune response can occur. Ultimately, this reaction results in excessive inflammation of the skin, as demonstrated by the aforementioned rash. Current research examines exactly how these DCs are activated in the first place.
Research has discovered that the purinergic receptor, P2X7, a ligand-gated ion channel expressed on DCs that has been shown to play an important role in activating T cells. Specifically, it's been shown that ATP released from skin cells is capable of activating this receptor (2)and causing the release of IL-1β (3), a molecule important for the sensitization process mentioned earlier. This process also involves the NLRP3 inflammasome (a structure within the DC) though the exact mechanism is unclear. In Weber et al. 2010, the role of this ATP receptor, P2X7, in CHS and its specific mechanism of action is illuminated.
