Chemicals commonly found in skincare products are intended to avoid interactions with the part of the immune system responsible for triggering allergic inflammatory responses. However, allergic reactions to skincare products are common, so what mechanisms can be held responsible for this unintentional health issue?
Everyday Health estimates that up to 24 percent of Americans will experience allergic reactions involving their skin at some point in life, often due to chemical compounds in skincare products like lotion and makeup. This type of allergy is called allergic contact dermatitis, one type of allergic response characterized by chemical contact with human skin that is sensitized to that particular chemical. This condition causes an inflammatory response, and common stimuli include poison ivy, nickel, rubber, and cosmetics.
In any allergic or autoimmune response, T cells of the human immune system perceive certain chemicals as foreign objects, such as a particular chemical in a skincare product. Because of this recognition and labeling as “foreign,” the T cells set things in motion for an inflammatory immune response to target the foreign chemicals.
But before T cells are able to recognize chemicals and trigger an immune response, certain cellular interactions involving these chemicals must occur. Small chemical compounds in skincare products are designed to “lack the chemical groups needed for this reaction to occur,” and in theory they should subsequently be “invisible” to T cells. However, allergic reactions to skincare products do occur, so what’s happening in the body to trigger such reactions?
New research shows that CD1a molecules from immune cells in the outer layer of the skin, called Langerhans cells, are involved in reacting with skincare product chemicals to make them recognizable by T cells. Normally CD1a molecules do not interact with T cells because of a lipid barrier that results from CD1a lipid binding.
Researchers from the current study observed chemicals commonly associated with skincare products and allergic contact dermatitis binding CD1a molecules, ultimately stimulating a reaction with T cells.
Uncovering physiological mechanisms like chemical interactions with CD1a molecules can help scientists develop new ways to treat allergic contact dermatitis or prevent the allergic reactions from occurring in the first place. For example, CD1a-directed interactions between external chemicals from skincare products and T cells could be prevented by supplementing the skin with additional lipids to support the lipid barrier between CD1a and T cells. Until researchers identify more causes of allergic contact dermatitis, the only other solution to prevent allergic reactions would be to avoid contact with chemicals that are known to cause an allergic reaction for a particular individual.
Sources: Columbia University Irving Medical Center, Science Immunology, “Allergic Contact Dermatitis”
