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46 Cards in this Set

  • Front
  • Back
what are the 4 types of inappropriates immune response
anaphylactic
antibody dependent cytotoxic
immune complex mediated
cell mediated (delayed type)
what type of inappropriate immune reponse is the ppd test
cell mediated (delayed type)
what is the time course for anaphylactic
minutes
what is the time course for cell mediated (delayed type)
24hrs - 48 hrs
what is the time cource for immune complex mediated
3-8 hrs
what is the time course for antibody-dependent cytotoxic
minutes to hours
what is hypersensitivity
inappropriate or excessive immune response
what type of inapropriate response is Atopic disease seen in and what is the characteristic of it
anaphylactic

produce IgE instead of IgG
what type of disease is caused by allergy
atopic
in type 1 hypersensitivity what is the cause
reactions are due to excessive activation of TH2 cells and overproduction of IgE
what is the sequence of events that occurs in type 1 hypersensitivity
allergen taken up

TH0 commit to TH2 cells

IgE binds to FcEPSILONReceptor on mast cells

IgE cross linked allergen

MAST CELL DEGRANULATES
what are the TH2 factors and what do they do
IL4, 13, CD40 cause switching of B cells to IgE

IL10 - inhibits TH1 and IL1 response
how does anaphylaxis occur
allergen crosslinks FcEPSILONreceptor resulting in a signal sent into mast cell

within minutes: increase in release of preformed mediators (histamine)

within hours: cytokines, lipids released
what does histamine cause
smooth muscle contraction
mucous secretion

*these help to get ride of parasites in GI

vasodilation
edema
*help to get immune substances from circulation into tissues
what are leukotrienes, prostaglandins, PAF
lipid mediators
what do lipid mediators do
increase vascular permeability
smooth muscle contraction
chemotaxis
if the cellular infiltrate has CD4+ cells, monocytes, and eosinophils what type of hypersensitivity
type 1
what are the TH2 cytokines
IL4, 5, 13
what is allergic rhinitis
hay fever
what produces eosinophil attractants and what are some examples of these attractants
mast cells produce them

example:
RANTES, IL5, eotaxin
why is excessive or prolonged type 1 response damagining
because eosinophils adhere to vascular endothelium and secrete MAJOR BASIC PROTEINS (MBP) AND PEROXIDASE which cause damage
what are the main components of asthma
increased contractile response of airways to stimulus.

inflamed airways: cellular infiltrate (macrophages, eosinophils, TH2 cells are found in air ways)
in asthma what do cytokines released from TH2 cause
edema of airway
mucus hypersecretion (IL13)
bronchial hyperresponsiveness
why does hypotension occur in anaphylaxis
due to histamine which causes vasodilation throughout the body and therefore can't retain fluid in circulation b/c leaks into tissue and decrease in BP
what tests are used to test allergy
wheal and flare
RAST
RIST
ELISA
what does RIST measure
total amount of IgE
what does RAST measure
measures levels of IgE that react to a specefic substance
what does Wheal and Flare measure
poke person w/ needle containing small amount of substance you believe they are allergic to (earliset result in 30 mins)
what does ELISA measure
serum IgE levels
in type 1 hypersensitivity how can you modulate the immune response
for asthma give anti-IgE (Xolair) to try to lower IgE levels

desensitization w/ allergen to try to encourage TH1 response and reduce TH2 response

Mast Cell stabilization
Mediator antagonism
what is used as a mast cell stabalizer
sodium cromoglycate
what are the mediator antagonism used in type 1 therapy
leukotriene receptor antagonists
histamine receptor antagonists (antihistamine)
what does augmentation of cAMP levels do to people w/ asthma
cAMP helps to relax airway of smooth muscle
what can be done to increase cAMP
B2 agonist
decrease cAMP degradation (inhibit phosphodiesterase)
what can be used to decrease cAMP degradation
theophyline
what can be given to treat chronic inflammation in asthma patients
corticosteroids
what do corticosteroids do
reduce cytokine production
what is type 2 hypersensitivity caused by
presence of antibodies against a cell or tissue
in type 2 how are cells killed
ADCC
phagocytosis
complement dependent lysis
in type 2 how are cells killed by phagocytosis
Antibody binds to FcGAMMAReceptor on cell and causes phagocytosis
in type 2 how are cells killed by complement dependent lysis
ab bound to cell and activates complement (classical pathway) to produce C3b which can opsonize cell to get phagocytosis

and if activation of complement continues then MAC will form and lysis of cell occurs
in type 2 how are cells killed by ADCC
if Ab binds to cell NK cells have Fc receptors that recognize those Ab and will kill the cell
how does glycosylation of RBC surface protein (H substance) effect IgM production
glycosylated of H substance resembles bacteria antigen in our gut and due to this no IgM will be made to counter this antigen due to it resembling our blood type
what causes type 3
prolonged or excessive immune complexes or they build to fast
what do immune complexes do
activate complement
attract neutrophils
anaphylatoxins
directly activate macrophages
cause platelet aggregation
what is serum sickness
excess antigen