Immune Attack On Tissues: Hypersensitivity, Allergy And Transplant Rejection Flashcards
Type 1 hypersensitivity definition
Atopic allergy Immediate Anaphylaxis Antibody mediated Damage to self tissue triggered bŷ an adaptive immune response to non infectious agents
Immunity, allergy and autoimmunity: self or foreign
Material recognised->material damaged-> result
Foreign-> foreign-> immunity
Foreign-> self-> allergy
Self-> self-> autoimmunity
Type 1 hypersensitivy mechanism, immediate
Often harmless antigen reacts with specific IgE antibodies located on mast cells and basophils.
- > rapid release of preformed chemicals from mast cell
- > histamine-> vasoactive and inflammatory
- > Leukotrienes and prostaglandins-> vasodilation, smooth muscle spasm, vasopermeability, excessive epithelial secretion
Type 1 hypersensitivy mechanism, late
Chronic response
Antigen is presented to Th2 cells
-> produce IL-4
-> stimulates B cells to produce IgE ->IgE binds mast cells->IgE-mast cell complex -> if exposed to antigen again-> reaction
Also produce IL-5-> stimulates eosinophils
Chronic tissue damage as a result of cytokines and eosinophil products
Anaphylaxis
Systemic
Common allergens-> drugs, serums, venoms, peanuts
Route of entry-> intravenous or oral absorption
Responses-> edema, increased vasuclar permeability, tracheal occlusion, circulatory collapse, death
Acute widespread effects due to antigen reaching the blood stream
Acute urticaria
Wheal and flare
Allergens-> insect bites! allergy testing
Route of entry-> subcutaneous
Response-> local increase in blood flow and vascular permeability
Allergic rhinitis
Allergens-> pollens, dust mite faeces
Route of entry-> inhalation
Responses-> edema of nasal mucosa, irritation of nasal mucosa
Asthma
Allergens-> danders (cat), pollens, dust mite faeces
Route of entry-> inhalation
Responses-> bronchial constriction! increased mucous production! airway inflammation
Inflammatory mediators increase mucous production-> acute response
Cytokines and eosinophils-> chronic response
Food allergy
Allergen->foods
Route of entry-> oral
Response-> d and v, pruritis, urticaria (hives), anaphylaxis
Skin prick test
Tests for sensitivity to specific allergens by intra dermal exposure
-> induces a wheel and flare reaction if allergic
Immediate-> redness and inflammation 15-60mins
Immediate + late-> redness and inflammation, appearance of IgE and T cells at 4-12 hours, disappear after 48
Delayed-> no redness till 12-48 hrs after appearance of Th1 cells
Eczematous test-> redness at 15-60mins, IgE and Th2 at 12-48 hrs-> broken skin
Type II hypersensitivity definition
Circulating antibodies attaching to specific body antigens leading to death of the cells and tissues bearing the specific antigen
Type II hypersensitivity mechanism
IgG, IgA or IgM antibodies bind to cell surface antigens
Results in antibody coated cells
Induces damage either by:
Lysis via activation of the complement system, cells can’t be phagocytosed so neutrophils secrete lysosomes
Or by killer cells directed against antibody covered cells
May also be phagocytosed by macrophages
Requires at least two IgG bound to target.
Examples of type II hypersensitivity
-Immune haemolytic anaemia: Allergic haemolytic anaemia Autoimmune haemolytic anaemia Blood transfusion reactions Haemolytic disease of new born Drug induced-> IgG specific for drugs that bind to the surface of RBC allergy. -autoimmune thrombocytopenia -pemphigold (skin) -goodpastures disease -myasthenia gravis -Graves' disease
Type III hypersensitivity, definition
A normal response becomes excessive
Deposition of soluble circulating antigen-antibody complexes in vessel walls or other tissues
Characterised by vasculitis-> firbinoid necrosis of small blood vessel walls
Low blood complement
Small complexes excredted
Type III hypersensitivity, mechanism
Several soluble antigens and antibodies cross link to form a lattice-> immune complex
Immune complex becomes lodged in tissues when too much is produced and can’t be removed fast enough
-> activate complement-> attract neutrophils
Neutrophils and factors attracted by platelets initiate the damage-> tissue inflammation and necrosis