Hypersensitivity Part 2 Flashcards
What is Goodpasture’s Syndrome?
- when IgG binds to a self-component causing a type II hypersensitivity reaction
- antibodies bind to basement membrane collagen type IV
- causes glomerulonephritis in the kidney and pulmonary haemorrhage in the lung
Describe what can happen to a person with a penicillin allergy
- type II hypersensitivity reaction
- penicillin binds to components of RBC membrane
- can form a complex which is taken up by macrophages
- complex can form neo-antigen which activates T cells that interact with B cells and antigen presenting cells to drive forward antibodies that recognise penicillin RBC complex
- immunoglobulins bind to RBC when penicillin is bound resulting in complement activation causing:
- lysis of RBCs
- binds to Fc receptor on macrophage to cause phagocytosis
What is responsible for clearing type III hypersensitivity reactions and what causes pathology?
- cleared by reticuloendothelial system (macrophages, neutrophils in liver spleen and bone marrow that ingest and degrade immune complexes)
- pathology is caused by excess immune complex deposition in tissues
Describe the progression of a type III hypersensitivity reaction
- locally injected antigen in immune individual with IgG antibody
- local immune-complex formation
- activation of complement release inflammatory mediators and induces mast cell degranulation
- causes local inflammation, movement of fluid and protein into tissue and blood vessel occlusion
What are the sites of type III immune complex depositon?
- glomeruli of kidney
- blood vessel walls: accumulates on veins and arteries causing vasculitis
- synovial membranes: RA can develop (when IgG of immune complexes becomes antigen itselg)
- skin: causes rashes
- systemic sites: if systemic lupus erythematosus it deposits in kidney, joints, skin, vasculature, muscle and other organs
What causes the majority of type IV hypersensitivity reactions?
- delayed type hypersensitivity reactions (DTH)
- some can be prolonged and damaging (eg. listerial and TB)
- can lead to walling off infectious sites, granuloma
Describe the progression of a type IV hypersensitivity reaction
- antigen introduced into subcutaneous tissue and processed by local antigen-presenting cells
- a TH1 effector cell recognises antigen and releases cytokines which act on vascular endothelium
- results in recruitment of T cells, phagocytes, fluid and proteins to site of antigen injections to cause lesion
What are contact sensitivities?
- a special category of DTH reaction in which antigen is not infectious but a chemical that binds to cell surface
- eg. heavy metal sensitivity and poison Ivy
Describe examples of autoimmune diseases that can be classified according to type II hypersensitivity reactions
- haemolytic anaemia: caused by blood group antigens resulting in destruction of rbc causing anaemia
- acute rheumatic fever caused by strep cell wall autoantigen (Ab x-react to cardiac muscle) causing arthritis, myocarditis and valve scarring
Describe examples of autoimmune diseases that can be classified according to type III hypersensitivity reactions
- SLE caused by DNA/histones/ribosome autoantigens resulting in glomerulonephritis, vasculitis and rash
- RA caused by rheumatoid factor IgG complexes resulting in arthritis
Describe examples of autoimmune diseases that can be classified according to type IV hypersensitivity reactions
- insulin dependent diabetes mellitus: caused by pancreatic B-cell antigen causing B-cell destruction
- RA: caused by synovial joint antigen resulting in joint inflammation and destruction