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As industries develop more chemical extraction techniques for synthetic or purified botanical ingredients to include in cosmetic and personal care products, the incidence of contact dermatitis is rising. Contact dermatitis (irritant or allergic) is the most common occupational skin disease, with current lifetime incidence exceeding 50%. For allergic contact dermatitis, type IV hypersensitivity (or delayed-type hypersensitivity) is thought to be the immunologic mediated pathway in which a T cell–mediated response occurs approximately 72 hours after exposure to the contact allergen. Diagnosis currently is predominately made clinically, after identifying the potential allergen or via patch testing. Treatment typically involves topical steroids or anti-inflammatories should a rash occur, and avoidance of the identified allergen.
In delayed-type hypersensitivity, most T-cell receptors recognize a peptide antigen bound to major histocompatibility complex (MHC) I or MHC II proteins, which stimulates a subsequent inflammatory immune response. However, in a recently published study, the authors wrote that “most known contact allergens are nonpeptidic small molecules, cations, or metals that are typically delivered to skin as drugs, oils, cosmetics, skin creams, or fragrances.” The chemical nature and structure of contact allergens “does not match the chemical structures of most antigens commonly recognized within the TCR-peptide-MHC axis,” they added. Thus, the mechanism by which nonpeptide molecules found in cosmetics cause a T cell–mediated hypersensitivity is poorly understood.
In that study, investigators from Brigham and Women’s Hospital, Boston; Columbia University, New York; and Monash University, Melbourne, looked at whether a protein found in immune cells – CD1a – could be involved in these allergic reactions. In a press release describing the results, cosenior author D. Branch Moody, MD, a principal investigator and physician in Brigham and Women’s division of rheumatology, inflammation, and immunity, noted that they “questioned the prevailing paradigm that T cell–mediated allergic reaction is only triggered when T cells respond to proteins or peptide antigens,” and found “a mechanism through which fragrance can initiate a T-cell response through a protein called CD1a.”
In their study, CD1a was identified as the and personal care products. Specifically, balsam of Peru (a tree oil commonly found in cosmetics and toothpaste), benzyl benzoate, benzyl cinnamate, and farnesol (often present in “fragrance”) after positive patch tests were found to elicit a CD1a-mediated immune response. Their findings suggest that, for these hydrophobic contact allergens, in forming CD1a-farnesol (or other) complexes, displacement of self-lipids normally bound to CD1a occurs, exposing T cell–stimulatory surface regions of CD1a that are normally hidden, thereby eliciting T cell–mediated hypersensitivity reactions.
The authors note that having a better understanding of how these ingredients elicit an immune response on a molecular level can help us potentially identify other molecules that can potentially block this response in humans, thereby treating or potentially mitigating allergic skin disease from these ingredients.
Dr. Wesley and Dr. Talakoub are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at dermnews@mdedge.com. They had no relevant disclosures.
Resource
Nicolai S et al. Sci Immunol. 2020 Jan 3. doi: 10.1126/sciimmunol.aax5430.
As industries develop more chemical extraction techniques for synthetic or purified botanical ingredients to include in cosmetic and personal care products, the incidence of contact dermatitis is rising. Contact dermatitis (irritant or allergic) is the most common occupational skin disease, with current lifetime incidence exceeding 50%. For allergic contact dermatitis, type IV hypersensitivity (or delayed-type hypersensitivity) is thought to be the immunologic mediated pathway in which a T cell–mediated response occurs approximately 72 hours after exposure to the contact allergen. Diagnosis currently is predominately made clinically, after identifying the potential allergen or via patch testing. Treatment typically involves topical steroids or anti-inflammatories should a rash occur, and avoidance of the identified allergen.
In delayed-type hypersensitivity, most T-cell receptors recognize a peptide antigen bound to major histocompatibility complex (MHC) I or MHC II proteins, which stimulates a subsequent inflammatory immune response. However, in a recently published study, the authors wrote that “most known contact allergens are nonpeptidic small molecules, cations, or metals that are typically delivered to skin as drugs, oils, cosmetics, skin creams, or fragrances.” The chemical nature and structure of contact allergens “does not match the chemical structures of most antigens commonly recognized within the TCR-peptide-MHC axis,” they added. Thus, the mechanism by which nonpeptide molecules found in cosmetics cause a T cell–mediated hypersensitivity is poorly understood.
In that study, investigators from Brigham and Women’s Hospital, Boston; Columbia University, New York; and Monash University, Melbourne, looked at whether a protein found in immune cells – CD1a – could be involved in these allergic reactions. In a press release describing the results, cosenior author D. Branch Moody, MD, a principal investigator and physician in Brigham and Women’s division of rheumatology, inflammation, and immunity, noted that they “questioned the prevailing paradigm that T cell–mediated allergic reaction is only triggered when T cells respond to proteins or peptide antigens,” and found “a mechanism through which fragrance can initiate a T-cell response through a protein called CD1a.”
In their study, CD1a was identified as the and personal care products. Specifically, balsam of Peru (a tree oil commonly found in cosmetics and toothpaste), benzyl benzoate, benzyl cinnamate, and farnesol (often present in “fragrance”) after positive patch tests were found to elicit a CD1a-mediated immune response. Their findings suggest that, for these hydrophobic contact allergens, in forming CD1a-farnesol (or other) complexes, displacement of self-lipids normally bound to CD1a occurs, exposing T cell–stimulatory surface regions of CD1a that are normally hidden, thereby eliciting T cell–mediated hypersensitivity reactions.
The authors note that having a better understanding of how these ingredients elicit an immune response on a molecular level can help us potentially identify other molecules that can potentially block this response in humans, thereby treating or potentially mitigating allergic skin disease from these ingredients.
Dr. Wesley and Dr. Talakoub are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at dermnews@mdedge.com. They had no relevant disclosures.
Resource
Nicolai S et al. Sci Immunol. 2020 Jan 3. doi: 10.1126/sciimmunol.aax5430.
As industries develop more chemical extraction techniques for synthetic or purified botanical ingredients to include in cosmetic and personal care products, the incidence of contact dermatitis is rising. Contact dermatitis (irritant or allergic) is the most common occupational skin disease, with current lifetime incidence exceeding 50%. For allergic contact dermatitis, type IV hypersensitivity (or delayed-type hypersensitivity) is thought to be the immunologic mediated pathway in which a T cell–mediated response occurs approximately 72 hours after exposure to the contact allergen. Diagnosis currently is predominately made clinically, after identifying the potential allergen or via patch testing. Treatment typically involves topical steroids or anti-inflammatories should a rash occur, and avoidance of the identified allergen.
In delayed-type hypersensitivity, most T-cell receptors recognize a peptide antigen bound to major histocompatibility complex (MHC) I or MHC II proteins, which stimulates a subsequent inflammatory immune response. However, in a recently published study, the authors wrote that “most known contact allergens are nonpeptidic small molecules, cations, or metals that are typically delivered to skin as drugs, oils, cosmetics, skin creams, or fragrances.” The chemical nature and structure of contact allergens “does not match the chemical structures of most antigens commonly recognized within the TCR-peptide-MHC axis,” they added. Thus, the mechanism by which nonpeptide molecules found in cosmetics cause a T cell–mediated hypersensitivity is poorly understood.
In that study, investigators from Brigham and Women’s Hospital, Boston; Columbia University, New York; and Monash University, Melbourne, looked at whether a protein found in immune cells – CD1a – could be involved in these allergic reactions. In a press release describing the results, cosenior author D. Branch Moody, MD, a principal investigator and physician in Brigham and Women’s division of rheumatology, inflammation, and immunity, noted that they “questioned the prevailing paradigm that T cell–mediated allergic reaction is only triggered when T cells respond to proteins or peptide antigens,” and found “a mechanism through which fragrance can initiate a T-cell response through a protein called CD1a.”
In their study, CD1a was identified as the and personal care products. Specifically, balsam of Peru (a tree oil commonly found in cosmetics and toothpaste), benzyl benzoate, benzyl cinnamate, and farnesol (often present in “fragrance”) after positive patch tests were found to elicit a CD1a-mediated immune response. Their findings suggest that, for these hydrophobic contact allergens, in forming CD1a-farnesol (or other) complexes, displacement of self-lipids normally bound to CD1a occurs, exposing T cell–stimulatory surface regions of CD1a that are normally hidden, thereby eliciting T cell–mediated hypersensitivity reactions.
The authors note that having a better understanding of how these ingredients elicit an immune response on a molecular level can help us potentially identify other molecules that can potentially block this response in humans, thereby treating or potentially mitigating allergic skin disease from these ingredients.
Dr. Wesley and Dr. Talakoub are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at dermnews@mdedge.com. They had no relevant disclosures.
Resource
Nicolai S et al. Sci Immunol. 2020 Jan 3. doi: 10.1126/sciimmunol.aax5430.