Desmosome (desmoglein 1 and 3)

Adhesion & dermo-epidermal junction · Dsg1 superficial Dsg3 deep Pemphigus

Keratinocyte-to-keratinocyte adhesion plaque in which desmoglein and desmocollin cadherins bind across the intercellular space and link through plakoglobin and desmoplakin to the keratin cytoskeleton. Which desmoglein is attacked determines how deep the blister forms.

Traced from the start

  1. Stratum basale (germinativum)Stratum spinosumStratum granulosum
  2. Desmosome (desmoglein 1 and 3)

Detail

Components
Desmoglein 1 and 3 plus desmocollins in the membrane; plakoglobin and desmoplakin in the plaque, tying to K5/K14 or K1/K10 filaments
Desmoglein distribution
In skin, Dsg1 predominates superficially and Dsg3 deeply; in mucosa Dsg3 predominates throughout with little Dsg1
Compensation rule
A desmoglein can be neutralised without blistering where the other one is co-expressed — this explains every pemphigus phenotype
Failure mode
Acantholysis: keratinocytes separate from one another while remaining attached to the basement membrane, giving flaccid blisters and a positive Nikolsky sign

When it goes wrong

IgG against Dsg3 alone (mucosal pemphigus vulgaris)

Painful, non-healing oral erosions that often precede skin disease by months; mucosa blisters because Dsg1 cannot compensate there

IgG against Dsg3 plus Dsg1 (mucocutaneous pemphigus vulgaris)

Suprabasal acantholysis with flaccid skin blisters and erosions as well as mucosal disease; direct immunofluorescence shows intercellular IgG and C3 throughout the epidermis; treated with corticosteroids and rituximab

IgG against Dsg1 alone (pemphigus foliaceus)

Subcorneal split at the granular layer with scaly crusted erosions on the trunk, face and scalp, and no mucosal involvement because Dsg3 compensates in mucosa

Practise this structure

16 questions in the bank tagged Skin.

All 16 Skin questions →