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Allergy & Autoimmunity - Allergic Contact Dermatitis
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Allergic contact dermatitis
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Allergic Contact DermatitisAcute ACD
- Edema
- Erythema
- Vesiculation
- Desquamation
- Infiltration
Patch testing » detection of contact allergens
ACD phases
Sensitization
1. Allergen-skin interaction
2. APC migration and maturation
3. T cell priming (in draining lymph node)
Elicitation
4. Inflammation (inflammatory cytokines)
1. Allergen-skin interaction
Skin penetration through the stratum corneum
Filaggrin in the skin barrier » defective skin barrier has NO filaggrin granules.
Filaggrin mutation frequent in Europeans and Asians.
Filaggrin mutation and increased skin irritability are risk factors for
polysensitization to fragrances.
Dendritic cells (DC)
Part of the innate immune system
Antigen presenting cells
Essential key-players for initiating adaptive immunity
Epidermal Langerhans cells
Binding to (cell-surface) proteins
Bonding: covalent to thiols, amines; coordinative
Metabolisation of pro-haptens: PPD » Bandrowski’s base
(para-phenyleendiamine (PPD) kan contact allergy reaction
veroorzaken)
Activation Langerhans cells:
Thiol group – NFkB & ERK1/2
Amino group – MAPK-p38
» result: modified cell surface receptor expression
TLR on dendritic cells (TLR-2 & 4)
PAMPS (pathogen associated molecular patterns), like LPS, viruses,..
Contributing to irritancy of allergens
“danger signal” » when allergen activate TLR-2 or 4
Nickel doesn’t activate the murine TLR4
Murine TLR4 has differences compared to human, missing histidines not
allowing nickel to bind to and stimulate TLR4 directly.
Hence, mice get hardly sensitized to nickel. Adjuvants (irritants) are needed!
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