Mechanisms of chemical-induced innate immunity in allergic contact dermatitis


  • Change made since online publication 21/05/2011: 3rd page ‘thereby prevents its ubiquitin conjugation’ changed to ‘thereby promotes its ubiquitin conjugation’. 14/06/2011

  • Edited by: Hans-Uwe Simon

Prof. Dr. Stefan F. Martin, Allergy Research Group, Department of Dermatology, University Medical Center Freiburg, Hauptstraße 7, D-79104 Freiburg, Germany.
Tel.: +49 761 270 67380
Fax: +49 761 270 66550


To cite this article:  Martin SF, Esser PR, Weber FC, Jakob T, Freudenberg MA, Schmidt M, Goebeler M. Invited review for the journal allergy mechanisms of chemical-induced innate immunity in allergic contact dermatitis. Allergy 2011; 66: 1152–1163.


Allergic contact dermatitis (ACD) is one of the most prevalent occupational skin diseases and causes severe and long-lasting health problems in the case of chronification. It is initiated by an innate inflammatory immune response to skin contact with low molecular weight chemicals that results in the priming of chemical-specific, skin-homing CD8+ Tc1/Tc17 and CD4+ Th1/Th17 cells. Following this sensitization step, T lymphocytes infiltrate the inflamed skin upon challenge with the same chemical. The T cells then exert cytotoxic function and secrete inflammatory mediators to produce an eczematous skin reaction. The recent characterization of the mechanisms underlying the innate inflammatory response has revealed that contact allergens activate innate effector mechanisms and signalling pathways that are also involved in anti-infectious immunity. This emerging analogy implies infection as a potential trigger or amplifier of the sensitization to contact allergens. Moreover, new mechanistic insights into the induction of ACD identify potential targets for preventive and therapeutic intervention. We summarize here the latest findings in this area of research.