Scientists have discovered a specific protein that causes allergic reactions when it comes into contact with odors that are common in cosmetic products.
It can cause immune cells to overdrive when people use skin creams, bodywashs, lotions, shampoos – and even toothpastes.
The breakthrough can help prevent rising cases of skin rashes, lumps, blisters, itchy eyes and facial swelling. It is called the “molecular missing link.”
An average woman uses 12 cosmetic items a day – with an estimated 168 different chemicals.
And while these products are becoming more common, scientists have noted that contact dermatitis – a type of allergic reaction that causes a red, itchy skin rash that hits certain substances – is also on the rise.
Contact dermatitis increases as the skin care and cosmetics industry grows. Now scientists understand how common odors activate a protein to cause the rash
The key protein, called CD1a, is located in immune cells that form the outermost layer of human skin. It offers hope for the development of drugs that block it.
Experiments showed that it binds directly to allergens or irritants in personal care products – thereby activating the T cells of the immune system.
These white blood cells kill foreign invaders. Allergies arise from a wrong identity when they respond to benign substances that would otherwise be harmless.
Co-lead author Professor David Branch Moody, from the Department of Rheumatology, Inflammation and Immunity at Brigham and Women’s Hospital in the United States, explained: “What we are presenting here is a molecular missing link.”
Compounds found in skin creams and other cosmetics can cause ACD (allergic contact dermatitis), he said.
The common situation is increasing, especially in the industrialized countries. But the exact reasons remain unclear.
Most allergies involving T cells are attributed to proteins or synthetically produced peptide antigens that activate the immune system.
But chemicals in personal care products are different types of molecules that were not thought to trigger an immediate reaction.
The latest findings, published in the journal Science Immunology, reveal how exactly components of daily consumer products do this.
They highlight the mystery behind the emergence of ACD, says the international team.
Prof. Moody said: “We have questioned the prevailing paradigm that T-cell mediated allergic response is only activated when T cells respond to proteins or peptide antigens.
“We find a mechanism by which odor can initiate a T-cell response via a protein called CD1a.”
Dermatologists have been wondering for years how allergies are caused by many substances in soap, cosmetics, fragrances, jewelry and plants.
The molecules were thought to be too small and had the wrong chemical structure to be detected directly by T cells – the immune cells that feed ACD.
Co-study leader Dr. Annemieke de Jong, skin immunologist at Columbia University, New York, and colleagues wondered if there could be another explanation.
So lead author Dr. Sarah Nicolai, MD, a medical researcher in Brigham, exposed T cells to material from test kits for skin patches used in allergy clinics.
This showed that they responded to certain substances, including Peruvian balm – widely used in cosmetics and toothpaste.
The researchers further identified ingredients in tree oil – benzyl benzoate and benzyl cinnamate – that were directly responsible for stimulating the reaction.
They also tested similar substances and found a dozen small molecules that seemed to elicit a reaction.
These include farnesol – an alcohol used in many products including deodorants, anti-aging creams, shower gels and shampoos.
Using scanning techniques, further analysis by researchers at Monash University, Melbourne showed that farnesol and CD1a are combined to destroy naturally occurring blood fats. This makes the protein more visible to T cells – thereby activating it.
The researchers are now planning to see if patients often have T cells that recognize molecules such as farnesol.
They are also looking for new molecules that can block the reaction of CD1a and cancel the activation of T cells. Work is currently being done to identify promising connections.