Immunopathology Flashcards
Type I hypersensitivity key features
-Antigens induc IgE
-IgE mediated mast cell degranulation
-Vascular leakage and eosinophil degranulation
-Histamine
-Immediate response
Mechanism of hypersensitivity type I
-Need prior exposure to an antigen stimulates production of antigen-specific IgE
-IgE binds to Fc receptors of mast cells and basophils-> crosslinks and causes cell degranulation
-Vasoactive mediators released into tissue
Manifestation of Typed I hypersensitivity
Allergens
-Gastrointestinal signs range from mild to severe
-1/2 food allergies cause skin atopy
Inhaled allergens
-Usually, atopic dermatitis
-some manifest in respiratory tract
Cutaneous allergens
Systemic manifestation-> anaphylaxis
Canine atopic dermatitis
Genetic predisposition that will alter where the lesions are.
-IgE antibody response to allergens
-Keratinocyte health and skin microbiome modulate response-promote and help the allergic response to happen more readily
-Filaggrin gene mutation found in atopy
-Look after skin health
Type II hypersensitivity
Cytotoxic reactions against cell membrane antigens
-Induce IgG or IgM
-Activate complement or leukocytes resulting in damage
Complement mediate mechanism
Antibody binds to cell membrane and classical complement cascade activate
-Formation of terminal membrane attack sequence and lysis
Leukocyte mediated mechanims
Leukocytes bind via Fc receptors
-Products damage membrane (lysosomal enzymes or oxygen free radicals)
Manifestation of type II hypersensitivity
-Circulating cells
React against RBC, leukocytes, platelets
-Epidermis
-Basement membrane
Glomerular or skin
Bovine neonatal pancytopenia
Calves develop pyrexia with external hemorrhage or death from internal hemorrhage (with fever)
-Found thrombocytopenia
-Destruction of hematopoietic cell lines in bone marrow
-Associated with BVD vaccine in cows lead to claves with pancytopenia
-Bovine MHC 1 molecules present in vaccine so make antibodies against this if a different type of MHC I
Type III hypersensitivities
-Form immune complexes with slight antigen excess (too small for phagocytes but too small to leave in urine)
-Complement and leukocytes induced tissue injury
-Reactions can occur to localized (arthus reaction) or circulating immune (serum sickness) complexes
Localized hypersensitivity
Interstitial antigen and intravascular antibody meet and precipitate within vessel walls
-Complement and leukocytes damage vessel and cause vascular necrosis, hemorrhage, thrombosis, and local tissue damgage
Systemic hypersensitivity
Soluble circulating immune complexes can be deposited within vessels can get stuck or get out through vessel
-Results in vasculitis, kidney, lungs(alveoli), joints, eyes
Infections canine hepatitis
Canine Adenovirus-1
-affinity for liver, kidney, eyes, and endothelial cells
-in young dogs
-Adequate antibodies clear the infections
-Later on see cloudiness in eyes and some respiratory signs
-Severe cases can see acute or chronic hepatitis, edema, blue eye
-Immune complexes causes uveitis and other eye issues, as well as glomerulonephritis and endothelium damage leading to DIC
Ocular lesions in Canine infectious hepatitis
Corneal edema due to antibody antigen complex binding to aqueous and endothelial cells and complement fixation will destroy cells and cause edema can recover after wards when complexes removed and endothelium regenerates
Type IV hypersensitivity
Cell mediated immune response
Persistent antigen
T-lymphocyte proliferation and lymphokine
macrophage proliferation and action
