Hypersensitivity Flashcards
hemolysis, anemia
Type II
Erythrocyte membrane proteins = Ag
Bleeding
Type II
platelet membrane proteins = Ag
nephritis, lung hemorrhage
Type II
Goodpasture’s syndrome
non-collagenous protein in basement membranes = Ag
hyperthyroidism
Type II
Thyroid stimulating hormone cells = Ag
Grave’s disease
muscle weakness/paralysis
Type II
acetylcholine using receptors
Myasthenia gravis
skin vesicles (bullae)
Type II
proteins in intracellular junctions of epidermal cells (cadherins) = Ag
Pemphigus vulgaris
Myocarditis, arthritis
Type II
Rheumatic fever
Streptococcal cell wall-Ab complex reacts with myocardial antigen
nephritis, arthritis, vasculitis
Type III
systemic lupus erythematosus
DNA, nucleoproteins, others
vasculitis
Type III
Polyarteritis nodos
microbial Ags
nephritis
Type III
post-streptococcal glomerulonephoritis
systemic vasculitis, nephritis, arthritis
Type III
serum sickness
cutaneous vasculitis
Type III
arthus reaction
What is seen in all Type III disorders?
injury is caused by complement mediated Fc receptor mediated inflammation, but the major mechanism of damage is classical activation of complement
Type IV hypersensitivity: major causes
autoimmunity, exaggerated/persistent response to environmental Ags
what cell mediates Type IV hypersensitivity?
T cells
what cell mechanism mediates type II hypersensitivity?
Ab mediated disease
what cell mechansism mediates type III hypersensitivity?
immune-complex disease
type IV sensitivity is caused by recruitment of what cells?
Th1
T IV HS is also called
Delayed Type Hypersensitivity
macrophage dependent tissue damage
T IV HS
brought on by Th1 memory
What HS rxns can be transferred, and what do they contain?
Type I, II, III can be transferred by serum containing Abs.
Type IV requires transfer of antigen specific Th1 clones that orchestrate MO response
Demyelination of the central nervous system, snensory motor dysfunction
T IV HS
Multiple sclerosis
myelin proteins = Ag
Inflammation of synovium, erosion of cartilage and bone joints
Rheumatoid arthritis
T IV HS
unknown antigens
Impaired glucose metabolism
T IV HS
Type I diabetes mellitus
inflammation of bowel wall, abdominal pain, diarrhea hemorrhage
T IV HS
Crohn’s disease
DTH reaction in skin
contact sensitivity
T IV HS
Chronic inflammation
chronic infections
T IV HS
DTH results from
activation of T cells, particularly CD4 cells
typically develops 24/48s hrs after Ag challenge
PPD
purified protein derivative of mycobacterium tuberculosis
elicits DTH rxn called tuberculin rxn
what 3 ways can humans be sensitized to DTH rxns?
microbial infection, contact sensitization, immunization
how many days do we expect primary DTH contact to produce outward symptoms?
none. takes 7-10 days, then requires re-exposure
