DefinitionThis section has been translated automatically.
Genetic factors influencing the predisposition or susceptibility to the development of contact allergy There is evidence that polymorphisms of the tumour necrosis factor genes (see tumour necrosis factor-α below), the filaggrin gene (see filaggrine below), the N-acetyltransferase genes NAT1 and NAT2 (see N-acetyltransferases), the glutathione S-transferase genes (see below glutathione S-transferases), the ACE genes (see below ACE) can influence the pathogenesis of the contact allergic reaction in different ways. Further polymorphisms in different cytokines, e.g. IL-16 (see below interleukins) also seem to play a role.
General informationThis section has been translated automatically.
- Nickel allergy has been particularly well studied with regard to genetic factors. Studies have shown that concordance is more pronounced in monozygotic twins than in dizygotic twins.
- The proportion of filaggrin mutations seems to be higher in nickel-contact sensitised twins than in other contact sensitised twins.
- It is worth noting that nickel is also directly recognised by T-cells during the process of contact sensitisation (also MHC-independent).
LiteratureThis section has been translated automatically.
- Bryld LE et al (2003) Risk factors influencing the development of hand eczema in a population-based twin sample. Br J Dermatol 149: 1214-1220
- Jensen CS et al (2002) Decrease in nickel sensitization in a Danish schoolgirl population with ears pierced after implementation of a nickel-exposure regulation. Br J Dermatol 146: 636-642
- Novak N et al (2008) Loss-of-function mutations in the filaggrin genes and allergic contact sensitization to nickel. J Invest Dermatol 128: 1430-1435
- Schnuch A (2011) Genetics of contact allergy. dermatologist 62: 732-738 -738