• Tight Junctions (Zonula Occludens)
    • Function: Prevents paracellular movement of solutes; maintains cellular polarity by separating apical from basolateral membrane spaces.
    • Components: Claudins, Occludins.
    • Location: Most apical junction.
    • Clinical Association:
      • Compromised in certain bacterial infections (e.g., C. perfringens enterotoxin affects claudins).
      • Blood-Brain Barrier integrity relies heavily on these.
  • Adherens Junctions (Zonula Adherens)
    • Function: Forms a “belt” connecting actin cytoskeletons of adjacent cells.
    • Components: E-cadherins (Ca2+-dependent adhesion proteins) connect to actin filaments via catenins.
    • Clinical Association:
      • Loss of E-cadherin promotes metastasis (allows tumor cells to detach and invade).
  • Desmosomes (Macula Adherens)
    • Function: Structural support via “spot welds”; anchors intermediate filaments (cytokeratin) of adjacent cells.
    • Components: Desmoglein, Desmocollin (members of the cadherin family).
    • Clinical Association:
      • Pemphigus Vulgaris: Autoantibodies (IgG) against Desmoglein (desmosomes).
        • Results in acantholysis (separation of keratinocytes).
        • Flaccid bullae, (+) Nikolsky sign, oral mucosa involvement.
        • Immunofluorescence: Net-like pattern around epidermal cells (“chicken wire”).
  • Gap Junctions
    • Function: Channel proteins that permit electrical and chemical communication between cells.
    • Components: Connexons (composed of 6 connexin subunits).
    • Clinical Association:
      • Critical in cardiac muscle (intercalated discs) for synchronized contraction.
      • Upregulated in myometrium before delivery (labor) to coordinate contractions.
  • Hemidesmosome
    • Function: Anchors the intermediate filaments of a basal epithelial cell to the underlying basement membrane. Connects Keratin in Basal cells to the Basement membrane.
    • Location: Basal surface of keratinocytes in the epidermis.
    • Key ProteinsIntegrins.
    • Clinical Correlation: Autoantibodies against hemidesmosomal proteins (e.g., BP180, BP230) cause Bullous pemphigoid, leading to subepidermal blistering.