Allergic Contact Dermatitis
The epidermal barrier is impaired in carriers of null mutations of the filaggrin gene (FLG). In accordance with this, all but one epidemiological study examining the association between FLG mutations and contact allergy (CA) identified a (slightly) increa
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Wolfgang J.C. Uter
Contents 23.1
Definitions and Background.......................
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23.2
Methods of Retrieval of Evidence ..............
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23.3
Results ..........................................................
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Conclusion ..............................................................
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References ...............................................................
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This chapter reviews evidence regarding the association between filaggrin gene (FLG) null mutations and allergic contact dermatitis (ACD) and contact allergy (CA), respectively. Hence, immediate-type hypersensitivity underlying contact urticaria, protein contact dermatitis, and extrinsic atopic eczema/dermatitis (AD) syndrome are not covered. After a brief definition of CA and ACD, the methods for retrieving evidence are described, an essential extract of available original data tabulated and discussed, finally arriving at a conclusion, which is considered valid at the time of writing. Obviously, new evidence in this emerging field of research will need to be considered in the future.
23.1
W.J.C. Uter, MD Department of Medical Informatics, Biometry and Epidemiology, University of Erlangen/Nürnberg, Waldstr. 4-6, Erlangen 91054, Germany e-mail: [email protected]
Definitions and Background
Contact allergy (CA, regarded here as synonymous with contact sensitization) is an acquired alteration of the immune system. CA occurs after an individual has been sufficiently exposed to a substance for sensitization to take place. While not all factors determining why a certain individual gets sensitized while another individual, exposed to a similar extent, does not get sensitized are fully understood, the general principle is well explored. Briefly, to be able to sensitize, the xenobiotic substance must be able (1) to penetrate the epidermal barrier; (2) to bind to skin (or, much more rarely, to mucous membrane) proteins, acting as a hapten, forming a full antigen with the protein; and (3) to mount a sufficient
J.P. Thyssen, H. Maibach (eds.), Filaggrin, DOI 10.1007/978-3-642-54379-1_23, © Springer-Verlag Berlin Heidelberg 2014
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activation of the dendritic cells and lymphocyte subsets involved, including a probably nonspecific “danger signal.” Components of both adaptive and innate immune systems are involved in this process [1, 2]. Recently, immunoregulation by regulatory T cells (Treg) has been identified as a major component of the sensitization process [3]. For a detailed description of this process, which is beyond the scope of this chapter, see, for example, the reviews cited above or [4]. Sensitization is not a “pass or fail” process, but a graded phenomenon, depending, among other factors, very much on the dose per area of exposure and on repetition of exposures: the higher the exposure dose is, not only the more likely the individual is to become sensitized but also the more intense the sensitization will be [5]. With repeated dosing, a super-additive effect has been noted [6]; that
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