Hypersensitivity (Bowden) Flashcards
(53 cards)
What is the Type I hypsersensitivity
Immediate (IgE)
3 properties of IgE control in Type I immediate Hypersensitivity
changes half life of IgE (binding IgE to cell R)
control of IgG and IgE production by T cells
Cross linking of IgE on surface of mast and basophils
Describe how Type I hypersensitivity is T cell dependent
Supressive Th1
Promotes Th2
class switch IL-4
What causes type I reactions
Allergens. usually protein
How are allergens classified
source, route and nature of protein
What are the classical allergens
low doses: inhaled about 1mg/yr
high doses: food (egg milk, nuts, fish)
What happens during repeated exposure to allergen
Mast cells release mediators
Types of mediators and when they are released
Preformed(under 5min) Histamine, heparin, and tryptase Newly Generated(5-30 min) Leukotrience D4, Arachidonic Acid, Prostaglandin D2 Cytokines take hours. IL-4 and TNFa
What are the symptoms/signs of mediators effects
Vascular leak, broncho-constriciton, intestinal hypermotility, inflammation, tissue damage, killing of parasites and host cells
How do we test allergies
Wheal and Flare reaction.
The wheal is the extravasation of sera
The flare is the axon reflex
What is a Late Phase Reaction
4-6 hours after initial Type I reaction. lasts 1-2 days
Infiltration of PMNs, eosinophils, macrophages, lymphocytes and basophils
what causes the late phase reaction
MAst cells produce TNFa and IL-1 leading to expression of adhesion molecules. Mast cells produce chemotactic IL8 and there is onsite release of IL-3 IL-5 IL-8 and GM-CSF (hematopoietic)
What is the Type II hypersensitivity
Antibody Mediated
What are the necessary components in Type II hs
IgG IgM FcR on effector cells and C’ and the surfaces that have the Ab
What are the IgM and IgG Abs binding to in Type II hs
“fixed Ag”
What are more pathogenic: Ab against cell surface Ag or internal Ag
Ab against cell surface Ags are usually pathogenic
What components from activated C’ system cause chemotaxis of PMNs, basophils and eosinophils
C3a and C5a
How does the Fc R communicate with the bound Ab in type II hs
either binds the Fc or binds bound C’ components
What do the effectors do in type II hs
Cytokine and chemokine by activated Eos, Neutrohils, NKs, Macrophages which release TNFa and IL1
Describe frustrated phagocyte
unable to take in the Ag so releases all its contents to kill it
what hemolytic disease occurs by type II hs
Hemolytic disease of newborn (Rh factor) also happens for blood types- more rare
Describe transfusion reaction
Fever, hypotension, nausea/vomiting, back&chest pain. donated blood- not whole blood unless emergency
Abs (IgM) will cause agglutination, C’a ctivation and intravascular hemolysis
Describe warm/cold Abs and what they assoc with
Autoimmune hemolytic anemias, type II hs.
warm: different epitopes then when transfused.
cold: high titer IgM- usually old people in winter.
How can drugs cause autoimmune hemolytic anemias
drugs bind RBCs and Ab to drug. Drug-Ab- immune complex gets absorbed by RBCs and is activated by C’ to be lysed.
