Hypersensitivity & Autoimmune Flashcards
type I hypersensitivity
immediate
allergen binds to allergen specific IgE antibody on mast cells leading to degranulation
type II hypersensitivity
antibody mediated
cytotoxic
immune response mediated by IgG antibodies directed against antigens on the surface of normal cells
type III hypersensitivity
immune complex mediated
IgM + IgG form complexes that deposit along the basal lamina and activate complement cascade
type IV hypersensitivity
cell mediated
delayed hypersensitivity reaction mediated by T cells
takes 1-3 days to see response
allergic hypersensitivity
adverse or unwanted immunologic response to allergens
pruritic skin disease resulting in self trauma and secondary lesions
immediate, late, or delayed
immediate reaction
develops in minutes
inflammatory mediators cause wheal formation
late phase reaction
develops in hours
inflammatory cells enter the tissue
delayed reaction
develops in hours/days
mediated by T cells
flea allergy dermatitis
hypersensitivity to proteins in flea saliva
occurs in dogs and cats
causes immediate and delayed reaction
FAD in dogs
lesions:
- alopecia
- erythema
- lichenification
- redundant skin folds
sites: caudal half of body, tail base, bilaterally symmetric
FAD in cats
highly variable lesions and presentation
erythematous eosinophilic plaques, rashes
miliary reaction
miliary reaction
inside –> out pattern of FAD in cats
tiny crusted pustules on the skin surface
culicoides hypersensitivity
hypersensitivity to the bites of culicoides fly species
occurs in HORSES with hereditary predisposition
dorsal and ventral disease pattern
culicoides lesion
dorsal: base of tail, rump, back, withers, crest, poll, ears
ventral: entire ventral midline
lesions: pruritus, excoriations, alopecia, lichenification
canine atopic dermatitis
transpidermal exposure and absorption of allergens through an epidermis with a defective barrier function
outside –> in process originating from decreased barrier function
steps of CAD development
- sensitization
- progression
- inflammation
sensitization
- defective barrier allows allergens to enter epidermis
- naive epidermal LCs capture and process antigens
- LCs migrate to local draining lymph nodes
- allergens are presented to naive Th lymphocytes and get activated to Th2 cells
- Th2 cells produce cytokines IL-4 and IL-13
- IL-4 and IL-13 stimulates B cell production of allergen specific IgE
- activated Th2 cells and AS IgE migrate to the dermis to begin role in the cycle of itch and inflammation
progression
- upon re-exposure to the same allergen, the epidermal LCs with cell surface bound AS IgE will bind allergen and migrate to the dermis
- AS IgE and LC cells present allergen to Th2 lymphocytes in the dermis
- allergens in the dermis trigger release of IL-31, pro-inflam cytokines, and histamine; activates sensory neurons to induce pruritus
inflammation
- pro-inflam cytokines recruit eosinophils and neutrophils to the dermis
- pruritus and inflammation cause the epidermis and stratum corneum to thicken, causing barrier function to worsen
- decreased barrier function allows increased allergen penetration –> repeats cycle
are autoimmune diseases common in animals
rare
diagnostic and treatment for autoimmune diseases
dx: skin biopsy
tx: immunosuppressive treatment
what do lesions of autoimmune diseases depend on
the target of the auto-antibodies and activated lymphocytes
ex. if target is melanocytes –> focal areas of depigmentation
what are the 3 classes of autoimmune disorders
- antibody mediated
- lymphocyte mediated
- antigen-antibody complex mediated
antibody mediated
targets: keratinocytes + BMZ
lymphocyte mediated
targets: keratinocytes, follicular bulb, melanocytes
antigen-antibody complex mediated
deposits immune complexes in the skin
pemphigus
antibody mediated autoimmune disease
auto-antibodies develop against transmembrane protein antigens required for keratinocyte adhesion
attacks desmosome proteins leading to loss of adhesion between keratinocytes
pemphigus foliaceus
autoantibodies against desmocollin 1 (DSC 1) in dogs
- unknown target in cats
pemphigus foliaceus lesion
large pustules and crusts
location: face (pinna, muzzle, nasal planum)
- NO oral mucosa lesions
- footpad and claw bed in cats
can cause systemic illness if generalized
pemphigus vulgaris
autoantibodies against desmoglein III (DSG III)
rare
pemphigus vulgaris lesions
coalescing erosions, ulcers, and vesicles
location: oral mucosa
often systemically ill
poor prognosis
