Abstract
Cosmetic products contain potential contact allergens or precursors that require metabolic conversion or oxidation to generate contact allergens. The most relevant contact allergens are fragrances and preservatives. These substances can pose hazards to human health due to their ability to activate T cells that can cause allergic contact dermatitis, an inflammatory skin disease. In recent years, much progress has been made in the elucidation of the mechanistic basis for immune system activation by contact allergens. This is essential for the development of better diagnostic tools, targeted therapies and animal-free in vitro assays for contact allergen identification. This overview will highlight some aspects of the activation of innate and adaptive immune responses by contact allergens.
Highlights
Cosmetic products contain potential contact allergens or precursors that require metabolic conversion or oxidation to generate contact allergens
These histidine residues are missing in the mouse TLR4, which explains the failure of nickel to induce allergic contact dermatitis (ACD) in the mouse contact hypersensitivity (CHS) model unless an adjuvant such as LPS is added
This study implies that contact allergens directly or indirectly engage an as-yet-unknown immunoreceptor tyrosine-based activation motif (ITAM) containing a receptor that signals via Syk
Summary
Contact allergens are small organic chemicals or metal ions As such they are too small to be recognized by the immune system. Chemical reactivity is the main feature that differentiates contact allergens from irritants The latter are, for example, detergents such as sodium dodecyl sulfate (SDS) that cause irritant contact dermatitis (ICD) but fail to activate an adaptive immune response. They exert toxic effects on skin cells and seem to evoke some aspects of the innate immune response. Repeated skin contact with the contact allergen may be required at the level of sensitization and elicitation for consumer or occupational ACD to occur. The immune response is rapidly downregulated by regulatory T cells and other cells with immunoregulatory functions such as NKT cells [9,11]
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