Basic Science of Skin and Cutaneous Immunology
Structure-function logic
The exam tests whether you can link anatomy to clinical signs. Know the epidermal layers and their keratins (K5/K14 basal, K1/K10 suprabasal, K6/K16 hyperproliferative), because genodermatosis questions hinge on which keratin or desmosomal protein is defective. Desmosomes (desmoglein 1 and 3, plakoglobin, desmoplakin) and hemidesmosomes (BPAG1, BPAG2/type XVII collagen, integrin α6β4) are the two adhesion systems examiners love to separate.
Immunology core
The skin immune system includes Langerhans cells (antigen presentation, CD1a+), dermal dendritic cells, mast cells, and resident memory T cells. Understand the Th1/Th2/Th17 axis: Th17 drives psoriasis and neutrophilic dermatoses, Th2 drives atopic dermatitis, Th1 drives granulomatous and type IV reactions. Complement, neutrophil chemotaxis, and the innate barrier (antimicrobial peptides, filaggrin) recur in questions.
Traps
- Confusing desmoglein 3 (mucosal-dominant pemphigus vulgaris) with desmoglein 1 (superficial pemphigus foliaceus).
- Assuming all type IV hypersensitivity is the same; nickel is Th1/IFN-γ, while atopic dermatitis is Th2/IL-4/IL-13.
- Forgetting that the dermo-epidermal junction has both hemidesmosomes and anchoring fibrils (type VII collagen, target in epidermolysis bullosa acquisita).
Rule of thumb
When a stem describes intraepidermal blistering, think desmosomes/keratins; when subepidermal, think hemidesmosomes/anchoring fibrils. Match the level of split to the protein.
Worked example
A neonate with generalized blistering and mucosal involvement, family history negative: absent staining for keratin 14 suggests epidermolysis bullosa simplex; absent type VII collagen suggests dystrophic EB. The level of cleavage on mapping is the discriminator.