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Review
. 2012 Jan 13;12(2):114-24.
doi: 10.1038/nri3150.

Early immune events in the induction of allergic contact dermatitis

Daniel H Kaplan  1 , Botond Z Igyártó, Anthony A Gaspari
Affiliations
Review

Early immune events in the induction of allergic contact dermatitis

Daniel H Kaplan et al. Nat Rev Immunol. .

Abstract

The skin is a barrier site that is exposed to a wide variety of potential pathogens. As in other organs, pathogens that invade the skin are recognized by pattern-recognition receptors (PRRs). Recently, it has been recognized that PRRs are also engaged by chemical contact allergens and, in susceptible individuals, this elicits an inappropriate immune response that results in allergic contact dermatitis. In this Review, we focus on how contact allergens promote inflammation by activating the innate immune system. We also examine how innate immune cells in the skin, including mast cells and dendritic cells, cooperate with each other and with T cells and keratinocytes to initiate and drive early responses to contact allergens.

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References

    1. Mowad CM. Patch testing: pitfalls and performance. Curr Opin Allergy Clin Immunol. 2006;6:340–4. - PubMed
    1. Thyssen JP, Linneberg A, Menne T, Johansen JD. The epidemiology of contact allergy in the general population--prevalence and main findings. Contact Dermatitis. 2007;57:287–99. - PubMed
    1. Diepgen TL. Occupational skin-disease data in Europe. Int Arch Occup Environ Health. 2003;76:331–8. - PubMed
    1. Diepgen TL, Coenraads PJ. The epidemiology of occupational contact dermatitis. Int Arch Occup Environ Health. 1999;72:496–506. - PubMed
    1. Martin SF. T lymphocyte-mediated immune responses to chemical haptens and metal ions: implications for allergic and autoimmune disease. Int Arch Allergy Immunol. 2004;134:186–98. - PubMed

Hightlighted References

    1. Landsteiner K, Jacobs J. Studies on the Sensitization of Animals with Simple Chemical Compounds : Iii. Anaphylaxis Induced by Arsphenamine. J Exp Med. 1936;64:717–21. Comment: This article first proposed the idea that the hapten-self complex is a critical early event in ACD. Seventy-five years later, this hypothesis has been supported by the work of many investigators, and remains a core concept of ACD.

    1. Martin SF, et al. Toll-like receptor and IL-12 signaling control susceptibility to contact hypersensitivity. J Exp Med. 2008;205:2151–62. Comment: This is the first article to suggest that innate immune receptors, in the form of TLR, play an important role in CHS

    1. Weber FC, et al. Lack of the purinergic receptor P2X(7) results in resistance to contact hypersensitivity. J Exp Med. 2010;207:2609–19. Comment: This study demonstrated that self-molecules (ATP) released as a result of cellular damage by haptens activates the inflammasome.

    1. Schmidt M, et al. Crucial role for human Toll-like receptor 4 in the development of contact allergy to nickel. Nat Immunol. 2010;11:814–9. Comment: This study demonstrated how the world’s most common contact allergen, Nickel, activates TLR-4, resulting in human APC activation upon exposure to this ubiquitious chemical.

    1. Itano AA, et al. Distinct dendritic cell populations sequentially present antigen to CD4 T cells and stimulate different aspects of cell-mediated immunity. Immunity. 2003;19:47–57. Comment: This study demonstrated that a productive immune response requires the transport antigen to the region lymph node by skin-resident dendritic cells.

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