We all know that a brush with poison ivy leaves us with an itchy painful rash. Now, Monash and Harvard researchers have discovered the molecular cause of this irritation. The finding brings us a step closer to designing agents to block this mechanism and sheds light on other serious skin conditions, such as psoriasis.
The international team of scientists have shown, for the first time, a connection between an immune molecule found in the skin and skin sensitisers – the research was published in Nature Immunology (doi: 10.1038/ni.3523).
Professor Jamie Rossjohn, co-lead author with Dr Florian Winau, Harvard Medical School, confirmed that the body’s immune molecule, CD1a, plays a crucial role in mediating skin inflammation and irritation after contact with urushiol – the active ingredient in plants endemic to Northern America and parts of Europe and Australia.
Dr Tang Yongqing and Dr Jerome Le Nours said the research team needed a combination of scientific creativity and ingenuity to crack the CD1a–urushiol code.
‘For over 35 years we have known CD1a is abundant in the skin,’ said Le Nours. ‘Its role in inflammatory skin disorders has been difficult to investigate and until now has been really unclear. Our work represents clear evidence that CD1a is instrumental in skin-related diseases. We are the first scientists to image the CD1a–urushiol connection.’
‘Our results were strengthened by in vivo and clinical studies at Harvard Medical School, in the United States,’ Yongqing said.
The studies in Boston also showed that blocking the function of CD1a prevents the triggering of this skin-based allergic reaction, giving the researchers further evidence of just how important CD1a is.
‘Future research could lead to the development of new treatments to combat minor skin irritations as well as chronic inflammatory skin diseases like psoriasis, eczema and rosacea,’ said Yongqing.