Zusammenfassung
Die Kontaktallergie ist eine Hauterkrankung, die durch die Reaktion des Immunsystems auf niedermolekulare Chemikalien verursacht wird. Kontaktallergene zeichnen sich durch chemische Reaktivität aus, die toxisch wirkenden Irritanzien fehlt. Kovalente Bindung von Kontaktallergenen an oder Komplexbildung mit Proteinen ist für die Aktivierung des Immunsystems unabdingbar. Als Konsequenz werden antigene Epitope gebildet, die von kontaktallergenspezifischen T-Zellen erkannt werden. Die Bildung von Effektor und Memory-T-Zellen bedingt die hohe Antigenspezifität und die wiederholte antigenspezifische Hautreaktion der Kontaktdermatitis. Neue Erkenntnisse zeigen, dass die weniger spezifische Reaktion des angeborenen Immunsystems auf Kontaktallergene der Reaktion auf eine Infektion sehr ähnlich ist. Somit handelt es sich bei der Kontaktallergie quasi um ein immunologisches Missverständnis, da der Hautkontakt mit Chemikalien als Infektion interpretiert wird. Das wachsende Verständnis der molekularen und zellulären Pathomechanismen der Kontaktallergie kann helfen, kausale Therapien und In-vitro-Alternativen zum Tierversuch für die Identifikation von Kontaktallergenen zu entwickeln.
Abstract
Contact allergy is a skin disease that is caused by the reaction of the immune system to low molecular weight chemicals. A hallmark of contact allergens is their chemical reactivity, which is not exhibited by toxic irritants. Covalent binding of contact allergens to or complex formation with proteins is essential for the activation of the immune system. As a consequence antigenic epitopes are formed, which are recognized by contact allergen-specific T cells. The generation of effector and memory T cells causes the high antigen specificity and the repeated antigen-specific skin reaction of contact allergy. New findings reveal that the less specific reaction of the innate immune system to contact allergens closely resembles the reaction to an infection. Therefore, contact allergy can be viewed as an immunologic misunderstanding since the skin contact with chemical allergens is interpreted as an infection. The growing understanding of the molecular and cellular pathologic mechanisms of contact allergy can aid the development of specific therapies and of in vitro alternatives to animal testing for the identification of contact allergens.
Abbreviations
- DAMPs:
-
Damage-assoziierte molekulare Muster
- DZ:
-
Dendritische Zelle
- HA:
-
Hyaluronsäure
- LLNA:
-
Local Lymph Node Assay
- LPS:
-
Lipopolysaccharid
- NLR:
-
NOD-like-Rezeptor
- PAMPs:
-
Pathogen-assoziierte molekulare Muster
- ROS:
-
Reaktive Sauerstoffspezies
- TNCB:
-
2,4,6-Trinitrochlorbenzol
- TLR:
-
Toll-like-Rezeptor
Literatur
Askenase PW, Majewska-Szczepanik M, Kerfoot S, Szczepanik M (2011) Participation of iNKT cells in the early and late components of Tc1-mediated DNFB contact sensitivity: cooperative role of gammadelta-T cells. Scand J Immunol 73:465–477
Basketter DA, Gerberick F, Kimber I (2007) The local lymph node assay and the assessment of relative potency: status of validation. Contact Dermatitis 57:70–75
Carbone T, Nasorri F, Pennino D et al (2010) CD56 highCD16 – NK cell involvement in cutaneous lichen planus. Eur J Dermatol 20:724–730
Cavani A (2008) T regulatory cells in contact hypersensitivity. Curr Opin Allergy Clin Immunol 8:294–298
Cavani A, De Luca A (2010) Allergic contact dermatitis: novel mechanisms and therapeutic perspectives. Curr Drug Metab 11:228–233
Dudeck A, Suender CA, Kostka SL et al (2011) Mast cells promote Th1 and Th17 responses by modulating dendritic cell maturation and function. Eur J Immunol 41:1883–1893
Engeman T, Gorbachev AV, Kish DD, Fairchild RL (2004) The intensity of neutrophil infiltration controls the number of antigen-primed CD8 T cells recruited into cutaneous antigen challenge sites. J Leukoc Biol 76:941–949
Geier J, Uter W, Krautheim A et al (2011) Die häufigsten Kontaktallergene der Jahre 2007–2009. Allergo J 20:93–101
Girardi M, Lewis J, Glusac E et al (2002) Resident skin-specific gammadelta T cells provide local, nonredundant regulation of cutaneous inflammation. J Exp Med 195:855–867
Gober MD, Fishelevich R, Zhao Y et al (2008) Human natural killer T cells infiltrate into the skin at elicitation sites of allergic contact dermatitis. J Invest Dermatol 128:1460–1469
Grimbaldeston MA, Nakae S, Kalesnikoff J, Tsai M, Galli SJ (2007) Mast cell-derived interleukin 10 limits skin pathology in contact dermatitis and chronic irradiation with ultraviolet B. Nat Immunol 8:1095–1104
Guan H, Zu G, Slater M, Elmets C, Xu H (2002) GammadeltaT cells regulate the development of hapten-specific CD8+ effector T cells in contact hypersensitivity responses. J Invest Dermatol 119:137–142
He D, Wu L, Kim HK et al (2009) IL-17 and IFN-gamma mediate the elicitation of contact hypersensitivity responses by different mechanisms and both are required for optimal responses. J Immunol 183:1463–1470
Jakob T, Pfender N, König T et al (2009) Langerhanszellbiologie im Wandel. Allergologie 32:462–468
Kawai T, Akira S (2010) The role of pattern-recognition receptors in innate immunity: update on Toll-like receptors. Nat Immunol 11:373–384
Kezic S (2011) Genetic susceptibility to occupational contact dermatitis. Int J Immunopathol Pharmacol 24:73S–78S
Kimber I, Basketter DA, Gerberick GF et al (2011) Chemical allergy: translating biology into hazard characterization. Toxicol Sci 120(Suppl 1):S238–S268
Kish DD, Li X, Fairchild RL (2009) CD8 T cells producing IL-17 and IFN-gamma initiate the innate immune response required for responses to antigen skin challenge. J Immunol 182:5949–5959
Martin SF, Dudda JC, Bachtanian E et al (2008) Toll-like receptor and IL-12 signaling control susceptibility to contact hypersensitivity. J Exp Med 205:2151–2162
Martin SF, Esser PR, Schmucker S et al (2010) T-cell recognition of chemicals, protein allergens and drugs: towards the development of in vitro assays. Cell Mol Life Sci 67:4171–4184
Martin SF, Esser PR, Weber FC et al (2011) Mechanisms of chemical-induced innate immunity in allergic contact dermatitis. Allergy 66:1152–1163
Martinon F, Mayor A, Tschopp J (2009) The inflammasomes: guardians of the body. Annu Rev Immunol 27:229–265
Paust S, Gill HS, Wang BZ et al. (2010) Critical role for the chemokine receptor CXCR6 in NK cell-mediated antigen-specific memory of haptens and viruses. Nat Immunol 11:1127–1135
Pennino D, Eyerich K, Scarponi C et al (2010) IL-17 amplifies human contact hypersensitivity by licensing hapten nonspecific Th1 cells to kill autologous keratinocytes. J Immunol 184:4880–4888
Sato N, Kinbara M, Kuroishi T et al (2007) Lipopolysaccharide promotes and augments metal allergies in mice, dependent on innate immunity and histidine decarboxylase. Clin Exp Allergy 37:743–751
Schmidt M, Raghavan B, Muller V et al (2010) Crucial role for human Toll-like receptor 4 in the development of contact allergy to nickel. Nat Immunol 11:814–819
Schnuch A, Westphal G, Mossner R et al (2011) Genetic factors in contact allergy – review and future goals. Contact Dermatitis 64:2–23
Vocanson M, Hennino A, Rozieres A et al (2009) Effector and regulatory mechanisms in allergic contact dermatitis. Allergy 64:1699–1714
Weber FC, Esser PR, Muller T et al (2010) Lack of the purinergic receptor P2X(7) results in resistance to contact hypersensitivity. J Exp Med 207:2609–2619
Zhao Y, Balato A, Fishelevich R et al (2009) Th17/Tc17 infiltration and associated cytokine gene expression in elicitation phase of allergic contact dermatitis. Br J Dermatol 161:1301–1306
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Martin, S. Immunologie der Kontaktallergie. Hautarzt 62, 739–743 (2011). https://doi.org/10.1007/s00105-011-2184-z
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DOI: https://doi.org/10.1007/s00105-011-2184-z