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36 Cards in this Set

  • Front
  • Back
Type I
igE mediates "allergy"
Type II
A/g mediated cytoticity
Type III
immune complex mediated
Type IV-
TL-mediated (DTH)
Cell mediated
Type 1 Details

2-30 minutes
Antigen crosslinking of igE on mast cells and basophils

Systemic anaphylaxis
(hay fever, asthma, food allergies)
type 2 Details
Antibody against cells

5-8 hours

Antibody+ complement generates ADCC (antibody dependent cell mediated cytotoxicity)

Blood transfusion reactions
rH reaction in fetus (blood group)
Type 3 Details
Immune complex

2-8 hours

antigen/antibody complexes deposited on tissue

Rheumatoid arthritis
Kidney damage
Type 4 Details

24-72 hours

th1 cytokines acting on macrophages

th1 macrophages

Tubercular lesions (lung scar tissues)
Basophil equivolents
Mast cells tissue equivalents
The antigen in type 1?
Type 1 has all the hallmarks of normal humoral response with exception of
igE is made
Sensitization in type 1
igE binds to high affinity Fc receptors

igE binds before antigen binds
Coated with igE before they see antigen
Antigen binding in type 1 causes what
clustering of Fc receptors


Mediators, which cause allergy sign and symptoms
Signs and symptoms of allergy
1) Increase in vascular permeability
2) Vasodilation
3) Smooth muscle contraction
Examples of allergans include
pollen:rye grass, ragweed
foods- shellfish, lactose,nuts, eggs
Insects- bee stings
Cells for type 1 reaction
Mast Cells

There are about 10k cubic millimeter skin
IgE binding Fc Receptors
1-2 times 10 minus 9
more than one antibody can bind to single antigen molecule

as FcReceptors are cross-linked
When receptors get close together, they also talk to each other.
Cross-talk leads to signal transduction (NFAT)

Calcium concentration increases

Causing degranulation
Physiological response to parasites
mechanism evolved
Parasites are usually polyvalent, meaning more than Ab can bind to antige nmolecule
Hypersentivity =
Histamine is the primary mediator
vascular permeability up
smooth muscle contraction up- trachae (asthma and hard to breath)

Histamine binds to receptors H1 receptor leading to type 1

Claratin is antihistamine binds to H1 receptor and prevents histamine binding
Secondary mediators of type 1- "allergy"
Leukotrienes LTB4
Prostaglandins PGE2
What to LTB4 and PgE2 do
Increase vascular permeability
Smooth muscleContraction increased

Mucus that calcium also triggers

Granules are mentioned
SYSTEMIC anaphylaxis
Shock like response
Within minutes of Type 1 Occurrence within "pre-sensitized" individual

Mast cells/basophils with igE on there.
B cells make antibody that binds to cells
Massive body wide degranulation
Massive degranulation during systemic anaphylaxis causes
VASOdilation throughout body

Blood pressure drops bc all the vessels have opened up.

Severed bronchi constriction- can't get enough air to survive---> suffocation
What is used to treat systemic anaphylaxis of type 1 allergy
EPINEPHRINE to reduce effects
= adrenaline

Sympathetic nervous system
decrease vascular permeability
Constrict blood vessels
Smooth muscle relaxation
What is local anaphylaxis?
Allergy rhinitis

Binds to mast cells in conjunctiva
Nasal mucosa- swell up and can't breathe---- Stuffy.

Asthma = Something near triggers, Lung tissues- bronchioles close out

Food allergies = goes into GI tract, crosslink iGE in gut --> consequences
Diarrhea or vomitting
Allergy Rhinitis
nasal irritation or inflammation. Symptoms of rhinitis include runny nose, itching, sneezing and stuffy nose due to blockage or congestion
Describe Type II response
Antibody mediated
5-8 hours
Ab + C'
Antibody dependent cell mediate cytotoxicity

example of blood transfusion and Rh reactions
Blood type differences
A= antibodies against B
AB= no antibodies
O= antibodies to A and B
Anti iGM complement- Rh+ molecule
Baby is rh+
Mother Rh-

IgM = no crossing when delivered
Mixing of mothers and baby's blood
IgM vs. igG
igG can cross center
Second baby with rh+
igG crosses center of placenta and destroys fetus (blood)
Type 3
Cross linking
Trying to clear out NEUTROPHILS

Neutrophils are first response fcR
Involve ROI (reactive oxidative intermediaries = pus)

Neutrophils are activated because of depositories

Ab-ag depositories in rheumatoid arthritis
Damages joint tissue
Type 4 DTH
th1 and cd4 IFN gamma

IFN gamma activates macrophages that destroy tissue

Destroy tissues that pathogen is in