An international team of researchers has finally decoded the science behind a plant responsible for no small degree of human misery: poison ivy.
For the first time, we now know why poison ivy leaves – the bane of campers, hikers, and overly curious kids alike – make us itch, and the answer lies in a key molecule called CD1a, which scientists have long known about but didn’t fully understand until now.
“For over 35 years we have known CD1a is abundant in the skin,” says researcher Jerome Le Nours from Monash University in Australia. “Its role in inflammatory skin disorders has been difficult to investigate and until now has been really unclear.”
One of the reasons for that lack of clarity has been that many experiments on skin disorders involve animal testing – specifically lab mice. And mice don’t produce CD1a, effectively creating a kind of ‘blind spot’ in the studies up to this point.
To get around this and examine whether CD1a might play a part in how human skin reacts when we brush up against poison ivy (Toxicodendron radicans) and similar rash-inducing plants, the researchers genetically engineered mice that did produce the molecule.
In doing so, the team found that CD1a – a protein that plays an important role in our immune systems – triggers a skin-based allergic reaction when we come into contact with urushiol, the allergen that functions as the active ingredient in plants like poison ivy, poison oak, and poison sumac.
When urushiol interacts with skin cells called Langerhans cells, the CD1a proteins (which are expressed by Langerhans cells) activate the immune system’s T cells. In turn, the T cells produce two proteins – interleukin 17 and interleukin 22 – which cause inflammation and itchiness.
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