Immune mediated skin disease Flashcards
(66 cards)
What are the two broad categories of immune-mediated skin disease?
Allergic skin disease and autoimmune skin disease
What is a common factor in immune-mediated skin disease?
Breakdown of immune tolerance
What causes allergies?
external antigens called allergens
examples:
- Flea allergic dermatitis – allergy to flea saliva
- Atopic dermatitis – allergy to dust mites, pollens & moulds
What causes immune mediated disease?
self-antigens
examples:
- Pemphigus foliaceus – destruction of desmosomal proteins
- Discoid lupus – damage to epidermal cells
- Sebaceous adenitis – destruction of sebaceous glands
What are common allergens that can trigger allergies?
What are common self-antigens that can trigger immune mediated skin disease?
What are the main causes of allergic skin diseases?
Multifactorial causes including:
- Genetics (e.g. canine atopic dermatitis in Labrador retrievers)
- Microbiome & antibiotics effects
- Exposure frequency (e.g. intermittent exposure often induces hypersensitivity)
- Skin barrier function
- Environmental chemicals
How does the hygiene hypothesis relate to allergic diseases?
Reduced microbial exposure in early life may impair immune tolerance, increasing susceptibility to allergies and autoimmune diseases
What role does the epithelial barrier hypothesis play in allergic diseases?
Disruption of skin barrier by environmental factors like detergents & microplastics may increase allergen penetration & immune activation
Define canine atopic dermatitis
Hereditary inflammatory skin disease
Typically pruritic (itchy)
Predominantly T-cell driven
Involves skin barrier abnormalities
Linked to allergen sensitisation
Associated with microbial dysbiosis
What are the three major clinical signs associated with allergic skin disease?
Pruritus
Urticaria
Plaque Formation
What are pruritogens, and how do they cause pruritus?
Pruritogens are itch-mediators produced by immune cells, including cytokines, chemokines & other mediators
They stimulate sensory nerves, leading to itching in allergic reactions
What type of hypersensitivity reaction is responsible for pruritus and urticaria in allergic skin disease, and which cells are involved?
Type I hypersensitivity, involving mast cells & basophils that release inflammatory mediators
What key mediators are released during a Type I hypersensitivity reaction, and what are their effects?
Histamine – Causes swelling & urticaria more than itch
Leukotriene B4, prostaglandins & proteases – Contribute to inflammation & itch
Nerve growth factor – Increases sensitivity to itch
IL-2 & IL-31 – Directly stimulate sensory nerves, enhancing pruritus
What is urticaria?
Skin reaction characterised by raised, swollen welts due to histamine release in Type I hypersensitivity response, commonly seen in allergic skin diseases
How does Type IV hypersensitivity contribute to pruritus in allergic skin disease?
T-helper (Th2-biased) lymphocytes release IL-31 (major cytokine that stimulates sensory nerves & induces itching) & other pro-inflammatory cytokines
What are the key steps in allergen sensitisation in dogs?
- Allergen Exposure – Allergen enters through skin, inhalation, ingestion, or injection (e.g. pollen, dust mites, flea saliva)
- Antigen Capture – Langerhans cells (APCs) capture & process allergen
- T-Helper Cell Activation – Th2 cells trigger allergic response (IgE production), while Th1 cells lead to non-allergic response (IgG)
- B-Cell Activation – Th2 cytokines (IL-4, IL-5, IL-13) signal B-cells to produce IgE
- Mast Cell Sensitisation – IgE binds to mast cells, priming them for future allergic reactions
What happens when an animal is re-exposed to an allergen?
- Allergen Recognition – immune system remembers allergen from previous exposure, with IgE antibodies already bound to mast cells
- IgE Cross-Linking – allergen binds to IgE on mast cells, triggering cross-linking of FcεRI receptors
- Mast Cell Degranulation – Histamine, leukotrienes, prostaglandins & cytokines are released, leading to inflammation
- Inflammatory Effects:
- Vasodilation → Redness & swelling
- Increased vascular permeability → Oedema (fluid leakage)
- Smooth muscle contraction → Bronchoconstriction (e.g. coughing, wheezing)
- Pruritus (itching) → Common in allergic dermatitis
- Immune Cell Recruitment → More inflammation, eosinophil involvement
What causes plaque formation (induration) in allergic skin disease?
Plaque formation is caused by Type IV hypersensitivity, where T-helper lymphocytes release cytokines:
Th1-biased response: IFNγ, TNFβ, IL-2, IL-3 → cellular infiltration, swelling & skin thickening
Th2 & Th17-biased response: IL-4, IL-5, IL-17 → eosinophilic granuloma complex
Lesions are usually pruritic
What role do haptens play in allergic skin disease?
Haptens are small molecules that, when bound to body proteins, create new immune targets, triggering contact hypersensitivity reactions
How does classical contact hypersensitivity present clinically?
It causes pruritic inflamed skin lesions that appear where allergen contacts body
Rare in small animals but seen in horses (e.g. from tack materials)
What are the subdivisions of allergic skin disease in dogs?
Food and environmental induced-atopic dermatitis
- e.g. house dust mites or food proteins
Flea allergy
Contact allergy
- e.g. drugs
How can food and environmental allergies be distinguished in dogs?
Malassezia increased in food allergy
Seasonality not seen in food allergy
Young age of onset for food
More compact age of onset for environmental allergy
GI signs more common in food allergy
What are the subdivisions of allergic skin disease in cats?
Feline atopic skin syndrome
Flea allergy
Insect and mite hypersensitivity
Food allergy
