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Nickel allergy

Nickel allergy
Specialty allergology, immunology
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Nickel allergy (also referred to as Ni-ACD) is a form of allergic contact dermatitis (ACD) caused by exposure to the chemical element nickel.

Nickel allergy results in a skin response after the skin comes in contact with an item that releases a large amount of nickel from its surface. The skin reaction can occur at the site of contact, or sometimes spread beyond to the rest of the body. Free (released) nickel that is able to penetrate the skin is taken up by scavenger (dendritic cells) and then presented to the immune system T-Cells. With each subsequent exposure to nickel these T cells become stimulated and duplicate (clone) themselves. With enough exposures to nickel, the amassing clones of T-cells reach 'threshold' and the skin develops a rash. The rash can present as acute, subacute, or chronic eczema-like skin patches, primarily at the site of contact with the nickel (e.g. earlobe from nickel earrings). From time of exposure the rash usually presents within 12–120 hours and can last for 3–4 weeks or for the continued duration of nickel contact/exposure.

Three simultaneous conditions must occur to trigger Ni-ACD: 1. Direct skin contact with nickel-releasing item. 2. Prolonged skin contact with nickel-releasing item. 3. A sufficient amount of nickel is released and absorbed into the skin to cause a reaction.

The pathophysiology is divided into induction elicitation phases. Induction is the critical phase (immunological event) when skin contact to nickel results in antigen presentation to the T cells, and T cell duplication (cloning) occurs. The metal cation Ni2+ is a low molecular weight hapten that easily penetrates the stratum corneum (top layer of skin). Nickel then binds to skin protein carriers creating an antigenic epitope. The determining factor in sensitization is exposure of significant amounts of "free nickel". This is important because different metal alloys release different amounts of free nickel. The antigenic epitope is collected by dermal dendritic cells and Langerhans cells, the antigen-presenting cells (APC) of the skin, and undergo maturation and migration to regional lymph nodes. The complex is predominantly expressed on (MHC) II, which activates and clonally expands naive CD4+ T cells. Upon re-exposure these now primed T cells will be activated and massively recruited to the skin, resulting in the elicitation phase and the clinical presentation of Ni-ACD.


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