Immune Molecule CD1a Seen as Skin Sensitizer, Tied to Poison Ivy and Other Skin Conditions

Skin Sensitizer

Some recent findings shed light on an immune molecule in the skin, called CD1a that marks progress in what has been a 35-year mystery. The molecule has been recognized as a skin sensitizer and its role in inflammation may have other implications for different types of skin conditions.

Although CD1a’s abundance in the skin has been known about for over three decades, exploring its potential role in skin inflammation has been tricky. This is because CD1a does not occur in mice, meaning there was no way to test whether any of the in vitro findings translated to how the molecule actually behaved in a living body. Through the use of “transgenic” mice that were artificially given the ability to express CD1a, this issue was bypassed.

The study itself focused on how CD1a reacted when exposed to urushiol, the active ingredient responsible for poison ivy’s itchy, painful rash, as well as other uncomfortable skin reactions caused by plants like poison oak. The use of imaging techniques allowed the researches to see CD1a reacting with urushiol to produce inflammation in the skin. The reaction also produced a cytokine (immune cell) signature that was seen in human subjects who were undergoing poison ivy reactions.

Some studies in Boston also showed that the blocking of CD1a prevented the poison ivy reaction from occurring, adding more evidence to the idea that the molecule played a central role in the process.

Although the study confined itself to CD1a’s role in urushiol-triggered reactions, the findings do have implications for other types of skin conditions. The immune molecule is a skin sensitizer, so it has the potential to show similar involvement in more serious skin conditions like psoriasis, which causes the development and shedding of skin plaques. Research into other inflammation-linked skin disorders, like rosacea or eczema, may also benefit from looking in to CD1a.

Kim., J., et. al., “CD1a on Langerhans cells controls inflammatory skin disease,” Nature Immunology, 2016; 10.1038/ni.3523.