Cutaneous Immunology

On this page

Cutaneous Immunology - Skin's Guardian Squad

Skin immune system cells and layers

  • Skin-Associated Lymphoid Tissue (SALT): Integrated system for cutaneous immune surveillance.
  • Innate Immunity (Rapid Defense):
    • Keratinocytes: Barrier; cytokines (IL-1, TNF-α), antimicrobial peptides (AMPs).
    • Langerhans Cells (LCs): Epidermal dendritic cells; potent antigen-presenting cells (APCs).
    • Others: Dermal Dendritic Cells (DDCs), Macrophages, Mast cells, NK cells.
  • Adaptive Immunity (Specific & Memory):
    • T-lymphocytes: CD4+ Helper (Th1, Th2, Th17, Treg), CD8+ Cytotoxic.
    • B-lymphocytes: Antibody production via plasma cells.
  • Key Cytokines (Cellular Messengers):
    • Pro-inflammatory: TNF-α, IL-1, IL-6, IL-17, IFN-γ.
    • Anti-inflammatory: IL-10, TGF-β.

⭐ Langerhans cells, key epidermal APCs, uniquely contain Birbeck granules (tennis-racket shape on EM), crucial for initiating skin immune responses.

Cutaneous Immunology - Antigen Alert System

  • Skin's surveillance: Detects pathogens via Pattern Recognition Receptors (PRRs) e.g., Toll-like Receptors (TLRs).
  • Key Antigen Presenting Cells (APCs):
    • Langerhans Cells (LCs): Epidermal; migrate to lymph nodes.
    • Dermal Dendritic Cells (DDCs): In dermis.
    • Keratinocytes: Can express MHC-II; produce cytokines (TNF-α, IL-1).
  • Process: APCs capture, process, and present antigens on MHC molecules to T-cells, initiating adaptive immunity. Migration of skin dendritic cells to lymph node

⭐ Langerhans cells uniquely contain Birbeck granules (tennis-racket shaped organelles on EM) and express CD1a & Langerin (CD207). 📌 Birbeck = Tennis Racket shape on EM for LCs!

Cutaneous Immunology - Itch & Scratch Saga

  • Hypersensitivity Reactions: Immune overreactions causing tissue damage & pruritus. 📌 Mnemonic: ACID
    • Type I (A - Allergic/Anaphylactic): IgE-mediated; mast cell degranulation (histamine).
      • Urticaria, angioedema. Intense itch.
    • Type II (C - Cytotoxic): IgG/IgM vs. cell-bound antigens.
      • Ex: Pemphigus.
    • Type III (I - Immune Complex): Ag-Ab complex deposition.
      • Ex: Cutaneous vasculitis.
    • Type IV (D - Delayed): T-cell mediated (Th1, CTLs).
      • Ex: Allergic contact dermatitis (ACD). ACD: severe itch.
  • Pruritus Mediators: Histamine, serotonin, Prostaglandins (PGs), Leukotrienes (LTs), Substance P, IL-31.
  • Itch-Scratch Cycle: Itch → Scratch → Skin barrier disruption → Inflammation → ↑Itch → Lichenification. Allergic Contact Dermatitis Overview

⭐ Type IV hypersensitivity is the mechanism behind allergic contact dermatitis, a common cause of severe, T-cell driven itch and eczematous skin changes.

Cutaneous Immunology - Self-Sabotage Stories

  • Autoimmunity: Immune system attacks skin's self-antigens due to failed self-tolerance.
  • Key Mediators:
    • Autoantibodies: Target skin structures (e.g., desmogleins in Pemphigus).
    • Autoreactive T-cells: Drive inflammation/damage (e.g., Lichen Planus).
    • Cytokines (TNF-α, IL-17): Amplify response.
  • Damage Mechanisms:
    • Type II Hypersensitivity: Antibody-driven (Pemphigus, Bullous Pemphigoid).
    • Type IV Hypersensitivity: Cell-mediated (Lichen Planus).
  • Common Autoimmune Skin Diseases:
    • Pemphigus Vulgaris (PV): Anti-desmoglein 3, 1. Intraepidermal.
    • Bullous Pemphigoid (BP): Anti-BPAG1 (BP230), BPAG2 (BP180). Subepidermal.
    • Lupus Erythematosus (LE): ANA, anti-dsDNA.
    • Dermatomyositis (DM): Anti-Mi-2, anti-Jo-1.

⭐ Pemphigus vulgaris often presents with oral mucosal erosions before skin lesions develop.

High‑Yield Points - ⚡ Biggest Takeaways

  • Langerhans cells: Epidermal APCs; crucial for initiating Type IV hypersensitivity.
  • Keratinocytes: Active source of cytokines (IL-1, TNF-α); contribute to innate and adaptive skin immunity.
  • Th1 cells: Mediate Delayed-Type Hypersensitivity (DTH) (e.g., contact dermatitis) via IFN-γ.
  • Th2 cells: Key in atopic dermatitis and urticaria, producing IL-4, IL-5, IL-13.
  • Mast cells: Release histamine and mediators in urticaria and anaphylaxis.
  • Autoantibodies: Anti-desmoglein (Pemphigus Vulgaris), anti-BPAG1/2 (Bullous Pemphigoid) are key markers.
  • CLA (Cutaneous Lymphocyte Antigen): Marker for skin-homing T lymphocytes.

Practice Questions: Cutaneous Immunology

Test your understanding with these related questions

What is the primary function of Langerhans' cells?

1 of 5

Flashcards: Cutaneous Immunology

1/10

Langerhans cells are positive for _____ and S100 on immunohistochemistry

TAP TO REVEAL ANSWER

Langerhans cells are positive for _____ and S100 on immunohistochemistry

CD1a

browseSpaceflip

Enjoying this lesson?

Get full access to all lessons, practice questions, and more.

Start Your Free Trial