Polysensitization and increased susceptibility in contact allergy: a review

Genetic factors presumably play a role in contact allergy (CA). There is, however, a lack of conclusive evidence from clinical studies. This may be on account of the strongly competing or modifying impact of exogenous factors, namely the potency of allergens and the intensity of exposure, and the fact that – in principle – everybody can be sensitized. Regarding phenotype, in contrast, polysensitization (PS) seems to indicate a subset of individuals at greater risk. In human sensitization experiments with dinitrochlorobenzene, induction was facilitated in PS, and elicitation enhanced. Recent clinical epidemiological data, taking confounders for PS, such as age, sex, and other skin diseases into account, demonstrated the following: (i) PS was the greatest risk factor to be sensitized to a number of (even weak) index allergens, indicating higher susceptibility on the level of induction; (ii) patch test reactions in PS patients were generally stronger indicating higher susceptibility on the level of elicitation. These findings are complemented by reports on polymorphisms of TNF‐α and IL‐16 in PS patients. Future studies on the genetics of CA should be performed in subgroups with PS, focussing on polymorphisms relevant for CA‐specific and nonspecific (inflammatory) processes.