Hypersensitivity Flashcards
hypersensitivity
inappropriate/heightened immune response to antigen
3 pillars
- cell mediated or humoral
- results in tissue injury
- pre-sensitized host. exposed to allergen once before.
type I hypersensitivity
immediate
AKA allergy
main effectors: mast cell/basophil; IgE; histamine
atopy
genetic predisposition to allergic reaction
abnormal IgE production; abnormal affinity of Ab to basophils
mechanism of injury - type 1
primary: body sees allergen, no reaction. b-cell sees antigen makes memory and plasma cells = IgE antibody.
secondary = second allergen present - allergen binds to sensitized mast cell = degranulation = release of histamine which causes effect of different parts of body
type 1 - primary mediators
deal with degranulation effect. key effects of immunological response.
- histamine
- serotonin
- eosinophils & neutrophils
- protease
type 1 - secondary mediators
make reaction last longer
- leukotrines
- PG
- bradykinin
- platelet activating factor
- cytokines
type II
antibody mediated hypersensitivity
type II main effectors & effector function of Ab
IgG IgM
complement
phagocytes
lyse bacterial walls trough MAC-Attack Complex
opsonie bacteria englulfed more readily
type II mechanism - secondary response
- bind allergen to surface of cell
- stimulation
- antibody bind to cell = immediate reaction
- opsonic phagocytosis & antibody dependent cellular cytotoxicity (ADCC) = influence lysis by protein. complement proteins activate - opsonization, increase phagocytes in area, MAC-Attack Complex.
Type II Disease
HDN - hemolytic disease of the newborn
Rh- mom and rh+ baby. first time IgG antibodies develop. nd rh+ baby - IgG Ab cross placenta and can attack baby. = inappropriate development.
treat = immunnoglobulin shot.
type III main effectors
immune complex hypersensitivity
main effectors: Ag-Ab complex; complement; inflammation
type III - physical responses & clinical manifestations
large complexes deposit in kidneys, microvasculature = vasculitis, nephritis, arthritis
local = arthus reaction = fungal spores inhaled, complex in lungs.
acute systemic = serum sickness - add wrong blood type into blood.
chronic systemic = SLE; rheumatoid arthitis
Type IV : main effectors
cell mediated: delayed.
CD8 t-cell = cytotoxic.
macrophage= infiltrate - injury to tissue
t-cell effector function
bacterium presents antigen - act on CD4 helper cell. with MHC complex.
cytotoxic CD8 cll kills cell thru activation of immune system. CD8 kills APC - which is CD4 in this case. osmotic lysis.
CD4 also act on their own - pre-cytotoxicity - to increase phagocytes, proliferate t-cell and increase edema ==> takes time. inflammation by phagocytes
clinical manifestation of type IV
contact dermatisis - poison ivy
chronic infectious diseases: viral hepititis
acute rejection of transplant
