hypersensitivities

Question 1

two ways effector mechanisms of inflammatory hypersensitivity type II are produced

Answer 1

complement mediated cytotoxity:

IgG and IgM activate complement through CP which produces C3a and C5a– results in inflammation

ab-dependent cellular cytoxicity (ADCC):

IgG binds to NK cells through FcRy receptors– causes conformational change in Fc receptor

Fc receptor activates neutrophils and macrophages which release inflammatory cytokines, ROS, lysosomal enzymes— damage adjacent tissues

Question 2

hypersensitvity reactions

Answer 2

cause tissue injury

also called immune-mediated inflammatory response

can arise from uncontrolled response to foreign ag or autoimmune against self ag

types I (immediate), II, III, IV (delayed)

Question 3

type I hypersensitivity overview

Answer 3

immediate

triggered by environmental ag

caused by mediators of mast cells which are activated by IgE

Question 4

atopy

Answer 4

genetic tendency to develop allergic diseases

Question 5

mast cell mediators and what they do

Answer 5

histamine- dilation of small vessels and vascular permeability

protease- local tissue damage

prostaglandin- vascular dilation

leukotrienes- smooth muscle contraction

cytokines- local inflammation (late phase reaction)

Question 6

initial allergen encounter

Answer 6

allergen enters body

Th2 cells and B cells that mature into plasma cells make IgE

IgE binds to FcRe (CD23) receptors on mast cells in tissues

Question 7

subsequent allergen encounter (secondary exposure)

Answer 7

ag dependent cross linking of mIgE activates mast cells to release their mediators

Question 8

times of reactions of hypersensitvity type 1

Answer 8

(immediate) within minutes: congestion, vasodilation, edema

(late phase) 2-24 hours: inflammatory infiltrate of eosinophils, neutrophils, T cells

Question 9

asthma

Answer 9

local reaction

release of inflammatory mediators from mast cells upon activation of ag

increased capillary permeability

spasmodic contraction of smooth muscle in bronchi, decreases size and causes shortness of breath

can also be triggered by colds and exercise

Question 10

anaphylaxis

Answer 10

systemic reaction (starts local)

massive release of vasoactive amines and cytokines that cause smooth muscle contraction and capillary endothelium vasodilation— caused by food allergen, large quantities of allergen

blood pressure drop causes vascular shock

bronchi constriction- difficult breathing

Question 11

type 1 hypersensitivity testing

Answer 11

standardized allergens injected into dermis

positive reaction indicated by swelling and redness within 20-30 minutes

Question 12

allergen specific immunotherapy (allergen-SIT)

Answer 12

single curative approach

administer increased doses of allergen

goals to produce:

• induced peripheral T cell tolerance
• thresholds for basophils and mast cell activation
• IgE- mediated histamine release

generation of induced regulatory FOXP3+CD4+CD25+ Treg cells are what is detected

Question 13

hypersensitivity without tissue inflammation

Answer 13

• abs bind to specific hormones or NT’s, stimulateing thyroid stimulating receptors, leading to hyperthyroidism (Grave’s disease)
• inhibit binding of aceytlcholine to ACh receptor leading to myasthenia gravis