Lecture 20

1.
What are hypersensitivity diseases?
Diseases caused by the immune system
2.
What mediates Type I HS?
IgE
3.
What kind of reaction does IgE cause?
Allergies
4.
"What type II, III HS mediated by?"
IgG
5.
What is Type IV HS mediated by?
Th cells
6.
What is Type IV HS also called?
Delayed type
7.
What is the term for someone who suffers from allergy?= =Atopic
8.
What is IgE an antibody response to?
Parasites
9.
What is characteristic of IgE response?
"Rapid, extensive"
10.
What is characteristic of mast cells relating to HS?
Large amount of IgE receptors - quick response
11.
What happens when an antibody bound mast cell binds pathogen?
Degranulation
12.
What is the problem with mast cells?
An allergen can stimulate degranulation
13.
What are the functions of granule mediators?
"Chemoattractants, activators, spasmogens"
14.
What do activators do?
"Increase blood flow, increase vasodilation"
15.
What do spasmogens do?
"Smooth muscle contraction, mucous"
16.
What are the preformed mast cell mediators?
"Histamines, tryptase"
17.
What is the advantage of preformed mediators?
Instant reaction
18.
What does tryptase do?
Cleaves components of ECM
19.
What are synthesised after degranulation?
"Lipid mediators, cytokines"
20.
What do lipid mediators do?
Smooth muscle contraction of blood vessels and enteric system
21.
What do cytokines like TNF do?
Stimulate inflammation
22.
What do histamines do?
"Vasodilation, permeability"
23.
What is the result of tryptase cleavage of ECM?
Tissue damage
24.
What are common allergens?
"Pollen, dust mites, venom, food allergies, penecillin, codeine/morphine"
25.
What happens to a second exposure to allergen by atopic individual?
Amplified response
26.
What happens during first exposure to an allergen or parasite?
Sensitises mast cells with IgE
27.
Where is IgE produced?
In the lymph nodes
28.
29.
What is it called when multiple sites have an allergic response?
Anaphylaxis
30.
What are treatments for allergies?
"Antihistamines, avoidance, steroids, norepinephrine, desensitisation"
31.
How is allergy tested?
"Skin prick, antibodies"
32.
Why might IgE give false negative?
IgE may be bound to mast cells and not show in blood
33.
What could be the cause of allergies?
Decrease of Tregs
34.
What could cause a decrease in Tregs?
Cleaner environment could have hindered Treg development
35.
What is the mechanism of Type II hypersensitivity?
Hemolytic anemia
36.
What is the mechanism behind hemolytic anemia?
"IgG coats RBCs, removed from circulation. IgM coats RBCs, lysed by complement"
37.
What can happen if antibodies bind tissue?
"Complement lysing, frustrated phagocytes"
38.
What do antibodies attack in good pastures syndrome?
Type IV collagen
39.
Where is type IV collagen found?
"Glomerular basement membrane, alveoli in the lungs"
40.
What are the symptoms of good pasture syndrome?
"Bleeding in the lungs, kidney dysfunction"
41.
What type of HS is caused by formation of antibody complexes?
Type III
42.
What type of hypersensitivity is rheumatoid arthritis?
Type III
43.
What type of HS is caused by formation of antibody complexes?
Type III
44.
Explain the mechanism of Type IV hypersensitivity?
Small molecule on skin => proteins carry to langerhan cell => langerhan cell to lymphnode => T cells to site => inflammation via cytokine release