IMMUNE BREAKTHROUGH: UNSCRATCHING POISON IVY’S RASH
MELBOURNE, MONDAY 22 AUGUST, 2016: 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 overnight in Nature Immunology (doi:10.1038/ni.3523).
Professor Jamie Rossjohn, co-lead author with Dr Florian Winau, Harvard Medical School, confirmed the body’s immune molecule, CD1a, plays a crucial role in mediating skin inflammation and irritation after contact with urushiol – the ‘active ingredient’ found in plants endemic to Northern America and parts of Europe and Australia.
“A complex set of experiments, coupled with imaging techniques at the Australian Synchrotron revealed the molecular interplay between CD1a and urushiol. This highlights CDIa’s role in sudden and uncomfortable skin reactions,” Professor Rossjohn says.
CRACKING A 35 YEAR MYSTERY
Dr Tang Yongqing and Dr Jerome Le Nours say 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,” says Dr 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,” Dr Yongqing says.
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,” says Dr Yongqing.
“We now have a target to further investigate. Our basic discovery may make a big difference in the future treatment and prevention of inflammatory skin diseases,” Dr Le Nours concludes.
This work was a collaboration between researchers from the Australian Research Council Centre of Excellence in Advanced Molecular Imaging at the Monash Biomedicine Discovery Institute (Rossjohn, Yongqing, Le Nours) and researchers at the Harvard Medical School (Winau).
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Dr Jerome Le Nours
Dr Tang Yongqing
Contact: Stephanie Pradier
0424 568 314
ARC Centre of Excellence in Advanced Molecular Imaging
The $39 million ARC-funded Imaging CoE develops and uses innovative imaging technologies to visualise the molecular interactions that underpin the immune system. Featuring an internationally renowned team of lead scientists across five major Australian Universities and academic and commercial partners globally, the Centre uses a truly multi scale and programmatic approach to imaging to deliver maximum impact.
The Imaging CoE is headquartered at Monash University with four collaborating organisations – La Trobe University, the University of Melbourne, University of New South Wales and the University of Queensland.
Monash Biomedicine Discovery Institute
Committed to making the discoveries that will relieve the future burden of disease, the newly established Monash Biomedicine Discovery Institute at Monash University brings together more than 100 internationally-renowned research teams. Our researchers are supported by world-class technology and infrastructure, and partner with industry, clinicians and researchers internationally to enhance lives through discovery.
Stylised image: Urushiol (in green), the ‘active ingredient’ in poison ivy, entrapped by CD1a molecule (in pink), which mediates the inflammatory response.