Hypersensitivity Flashcards
What is the immune reactant in type II hypersensitivity?
IgG
What is the immune reactant in type III hypersensitivity?
IgG
What is the immune reactant in type IV hypersensitivity?
Th1 cells, Th2 cells, CTL
What is the antigen associated with type II hypersensitivity?
Cell or matrix associated
Cell surface receptor
What are the properties of the antigens in type III sensitivity?
soluble
What are the properties of the antigens in type VI sensitivity?
Soluble
cell-associated antigen
What is the effector mechanism in type II hypersensitivity?
Complement
FcR and cell
Ab alters signalling
What is the effector mechanism in type III hypersensitivity?
complement
phagocytes
What is the effector mechanism in type VI hypersensitivity?
Macrophage activation
Eosinophil activation
cytotoxicity
Example of type II sensitivity
Drugs
Chronic urticaria
Example of type III sensitivity
Arthus reaction
Example of type IV sensitivity
contact dermatitis
tuberculin reaction
chronic asthma
allergic rhinitis
What are type II reactions a result of?
antibodies, usually IgG, binding to componenets of cell membranes or extracellular matrix
Can be self-components, or exogenous
What is a presentation of self-type II sensitivity?
Goodpasture’s syndrome
- antibodies bind to basemement membrane of collage type IV
- glomerulophritis in kidney
- haemorrhage in lung
- auditory canal and ears
What is haemolytic anaemia and what can it be caused by?
antibodies to substances bound to host cell surface
penicillin
Describe penicillin allergey
- penicillin modifies proteins on human RBC to create a foreign apltopose
- complement caoted penicillin modified RBCs are phagocytosed by macrophages using their complement receptors
- macrophages present peptides from penicillin-protein conjugate and activate specific CD4 T cells to become Th2 cells
- B cells are activate by antigen and by help from Th2 cells
- Plasma cells secrete penicillin specific IgG which binds to modified RBC
- Penicillin specific IgG binds to penicillin modified proteins on RBC
- Actuvation of complement causes lysis or phagocytosis of RBC
What antibodies cause type II hypersenstivity? And what is it?
IgG but sometimes IgM
directed to soluble antigen
excess immune complex deposition
What are the main sites of immune compelx deposition?
no necessarily from where the anitgen is derived
- glomeruli
- blood vessel walls
- synvoial membranes
- skin
- systemic sites
What is type IV hypersensitivty mediated by?
cell mediated
complement does not play a role
What are most type IV reactions caused by?
CD4+ delayed type hypersensitivyt (DTH) reactions
“delayed” =
2 - 4 days after exposure after antigen exposure
Examples of contact sensitivites
Chemical that binds to cell surface
- heavy metal sensitivity
- Poison ivy - reaction in the skin to catechols
Examples of type II hypersensitivty reactions
- autoimmune haemolytic anaemia - destruction of RBC
- Autoimmune thrombocytopenic purpure; platelet integrin, GpIIb:IIIa - abnormal bleeding
- Goodpasture’s syndrome; collagen type IV - glomerulonephritis, pulmonary haemorrhage
- Pemphigus vulagris; epidermal caherin - skin blisters
- acute rheumatic fever; strep cell wall - arthritis, myocarditis, valve scarring
Examples of type III hypersensitivity syndromes?
- mixed essential cryoglobulinemia - systemic vasculitis
- SLE - glomerulnephritis
- Rheumatoid arthritis - arthritis
Example of type IV sensitivity syndrome
- insulin dependent diabetes = beta cell destruction
- rheumatoid arthritis = joint destruction and inflammation
- MS = nervous system damage
Summary of each type of hypersensitivity
- Type II reactions: antibody mediated, cell membranes, drugs bound to cell membranes
- Type III: antibody mediated, immune complex formation to soluble antigens, deposits at key sites, kidney, vessels, joints, skin
- Type IV: cell mediated, DTH reactions to infectious organisms, granuloma. Contact sensitivity to reactive chemicals.
