DefinitionThis section has been translated automatically.
Antigen-specific, T-cell-mediated, delayed type IV immune response (Gell and Coombs) that occurs after repeated exposure to contact allergens. (see below allergy, type IV reaction) can occur in persons with the appropriate disposition. The predisposition can be based on genetic or non-genetic factors (see below contact allergy, genetics). Other non-specific factors such as infections can also be involved in the initiation of the contact allergic reaction.
The most frequent contact allergens are metal allergens(nickel) followed by cosmetics, creams, light protection agents and externally applied drugs. Typical for a contact allergic reaction are scattering reactions, which can often occur in the immediate vicinity of the contact site but also far away as a systemic scattering reaction.
Less frequent are so-called contact allergies of the immediate type (detection by atopy patch test), a type IV reaction triggered by type I allergens - here the most frequent triggers are plant and animal products.
Occurrence/EpidemiologyThis section has been translated automatically.
|Test substance (children)||Children (% positive)||Test substance (adults)||Adults (% positive)|
|Nickel sulphate||8,5||Nickel sulphate||11,5|
|Fragrance mix||5,5||Fragrance mix||8,4|
|Fragrance Mix II||3,1||Cobalt chloride||5,3|
|MCI/MI(Methylisothiazolinone)||2,2||Fragrance Mix II||5,0|
|Thiuram mix||2,1||Potassium dichromate||4,0|
Remarkably, a lower frequency of contact allergies is detectable in psoriatic patients (Claßen et al.2017).
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EtiopathogenesisThis section has been translated automatically.
Allergic contact dermatitis (contact eczema) is the prototype of a cell-mediated immune reaction of the late type (DTH = delayed-type hypersensitivity, type IV reaction according to Coobms and Gell). Basically, we believe that this reaction takes place in 2 phases:
- In the sensitization phase, keratinocytes and dermal mast cells are stimulated to produce large amounts of interleukin-1 and TNF-alpha shortly after application. These are responsible for the maturation of Langerhans cells into immunostimulating dendritic cells (DCs). Antigen-loaded dermal dendritic cells (DDCs) enter the draining lymph nodes. There they present naive T cells (see antigen presentation below) that carry the T cell receptor matching the antigen (or hapten-protein complex), the MHC antigen complex. This triggers a Th1/Tc1- and Th17/Tc17-predominant T-cell response.
- Haptens activate the ERK1/2 mitogen-activated protein kinase (see MAP kinase signalling pathway below) in human dendritic cells by binding to thiol groups. They also induce an increased expression of interleukin 1-beta mRNA. Hapten-activated keratinocytes express increased levels of TNF-alfa, IL-1ß, GM-CSF, chemokines, adhesion molecules (LFA-1 and ICAM-1, see integrins below).
- Langerhans cells activate the T-cell interaction of MHC I (major histocompatibility complex) or MHC II, which presents the hapten, with the hapten-specific T-cell receptor.
- Alternatively, the activation occurs via costimulatory molecules, e.g. B7-1, B7-2, ICAM-1. Both signals together lead to the activation and clonal expansion of hapten-specific CD4 and CD8 cells, which are able to migrate into the skin due to their pattern of adhesion molecules and chemokine receptors (specific homing).
Secondary antigen contact (trigger phase):
- Renewed contact with the same allergen leads to activation of antigen-specific memory cells. These develop into effector cells which initiate an inflammatory reaction (clinical: erythema, oedema, itching, vesiculation, desquamation; immunological: cytokine release, recruitment of further inflammatory cells). Immunological course: Specific T-memory cells, which are activated after renewed contact with the antigen and transform into effector cells, are initiators of the inflammatory reaction, but not its executors. CD4+ and CD8+ T cells are mainly involved in the trigger phase of AKD. The number of CD8 T cells increases in the skin 6-18 hours after contact with the hapten and is accompanied by an increase in IFN-gamma. Non-specific inflammatory cells (e.g. neutrophil granulocytes, mast cells, macrophages) act as executors.
- Recent contact with haptens leads directly and concentration-dependent to:
- increased expression of surface molecules and the production of cytokines by epidermal cells and endothelia. A certain non-specific irritant activity of the hapten is a prerequisite for the triggering of an allergic contact allergy.
- Recruitment of antigen-specific T cells to the site of Ag contact by inflammatory signals for the release of chemokines and cytokines from keratinocytes.
- Activation of endothelial cells, as the presentation of the antigen to T cells can only be done extravasally, and expression of adhesion molecules, e.g. E-, L-, P-selectin; ICAM-1, LFA-1, CD18.
Cutaneous inflammatory reaction:
- After hapten-specific activation, cytotoxic T-lymphocytes (CTL) lyse the hapten-modified (and thus attackable) keratinocytes. This leads to the release of inflammation mediators, recruitment of mononuclear cells and strengthening of the immune response. In addition, both TH1 and TH2 cells produce cytokines and mediators (e.g. INF gamma, TNF-alpha, IL-12), which locally also lead to an intensification of the reaction. Substance P and CGR-peptides (calcitonin gene related peptides) also act in the sense of an intensified inflammatory reaction. On the other hand, IL-4 and IL-10, which are produced by CD4+ TH2 cells and are involved in negative regulation of AKD, have an effect. This also applies to some neuropeptides, such as alpha-MSH and the vasoactive intestinal peptide (VIP).
- Antigen-specific T cells can stimulate local mast cells to produce TNF-alpha and MIP-2/IL-8. TNF-alpha induces expression of adhesion molecules that enable neutrophil granulocytes to bind to vascular endothelia. MIP-2/IL-8 establishes a chemotactic gradient that is responsible for transvasal diapedesis and targeted migration to the tissue loci contacted by haptene.
ManifestationThis section has been translated automatically.
Contact allergy is a widespread disease. 15-20% of the general population is sensitized to one of the common contact allergens. Manifestly, about 8% of adults and 5-6% of children fall ill once in a lifetime. Gender-specific differences are not found.
Note(s)This section has been translated automatically.
Current data on the incidence of allergic diseases in children show 12-month prevalence data for allergic rhinitis of 9.1%, atopic eczema of 6.0% and bronchial asthma of 4.1% (Worm M et al. ).
LiteratureThis section has been translated automatically.
Claßen A et al (2018) The frequency of specific contact allergies is reduced in patients withpsoriasis
. Br J Dermatol doi: 10.1111/bjd.17080.
Davies EE et al (2007) Para-phenylenediamine allergy from a henna tattoo. Arch Dis Child 92: 243
- Flint MS et al (2003) Differential regulation of sensitizer-induced inflammation and immunity by acute restraint stress in allergic contact dermatitis. J Neuroimmunol 140: 28-40
- Kawase Y et al (2003) Exacerbated and prolonged allergic and non-allergic inflammatory cutaneous reaction in mice with targeted interleukin-18 expression in the skin. J Invest Dermatol 121: 502-509
- Krüger U, Fuchs Th (2007) Contact urticaria and protein contact dermatitis in occupational dermatology. Derm Occupation and Environment 55: 107-111
- Marchese C et al (2003) Nickel-induced keratinocyte proliferation and up-modulation of the keratinocyte growth factor receptor expression. Exp Dermatol 12: 497-505
- Mascia F et al (2003) Blockade of the EGF receptor induces a deranged chemokine expression in keratinocytes leading to enhanced skin inflammation. At J cathode 163: 303-312
- Meingassner JG et al (2003) Pimecrolimus inhibits the elicitation phase but does not suppress the sensitization phase in murine contact hypersensitivity, in contrast to tacrolimus and cyclosporine A. J Invest Dermatol 121: 77-80
- Moulon C et al (2003) T cell receptor transfection shows non-HLA-restricted recognition of nickel by CD8+ human T cells to be mediated by alphabeta T cell receptors. J Invest Dermatol 121: 496-501
- Plitz, T et al (2003) IL-18 binding protein protects against contact hypersensitivity. J Immunol 171: 1164-1171
- Riemann H et al (2003) Pathomechanisms of the trigger phase of allergic contact dermatitis. JDDG 1: 613-619
- Schnuch A (2013) Genetics of contact allergy. dermatologist 62: 732-738
- Schnuch A et al. (2015) widespread disease contact allergy. dermatologist 66: 644-645
- Uter W et al (1999) The MOAHLFA index in 17 centers of the Information Network of Departments of Dermatology (IVDK) over 6 years. Contact Dermatitis 41: 343-344
- Wildemore JK et al (2003) Evaluation of the histologic characteristics of patch test confirmed allergic contact dermatitis. J Am Acad Dermatol 49: 243-248
- Zhai H et al (2003) Provocative use test of nickel coins in nickel-sensitized subjects and controls. Br J Dermatol 149: 311-317
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