14. hypersensitivity I Flashcards
what is hypersensitvity I reaction?
steps?
Why does IgE not remain long in plasma
what receptor does IgE bind on mast cells
what is sensitization?
what happens at the receptor upon subsequent exposure?
when (in time) is the late phase response?
does the mast cell constituitively express the FCERI receptor?
yes
how is IgG different than IgE?
binds FcyR after binding antigen
how do mast cell degranualation symptoms vary?
systemic?
what is wheal and flare?
what is urticaria?
what is pruritis?
what is D. pteronyssimus?
why is sensitization essential for type I hypersensitvity reactions? what cytokines drive TH2 developement? which cytokines drive B cell class switching?
which cytokines inhibit class switching
TH2 profile (IL-4, 5, 9, 13) –drives TH2 development & B cell IgE switch
KO CD40, IL-4, IL-13, STAT6 inhibit allergic reaction (essential in both T and B cells)
Which mediators in mast cells are preformed?
Which are newly synthesized?
where are mast cells located?
list all the classes of products and examples:
1. enzymes
2. toxic mediators
3. cytokines
4. Chemokine
5. Lipid mediator (interestingly, what do these do?)
- Found in mucosa and connective tissue where they function in host defense (helminth and tick infections)
- Biological activities mediated by preformed and newly synthesized mediators
Preformed:
Histamine: vasoactive increasing blood/permeability
enzymes: like mast cell chymase, tryptase, serine esterase which may activate matrix metalloproteinases –breakdown extra-cellular matrix
Newly synthesized:
a. Chemokines (inflammation)
b. Lipid mediators (>smooth muscle contraction, vasodilation, vascular permeability, mucus secretion)
c. cytokines (IL-3, IL-4, 5, 13) -sustain response that becomes amplified by recruited eosinophils, basophils, and Th2
d. TNFa (preformed also): activates endothelium-adhesion molecules upregulated -influx of leukocytes- inflammed so Leuk stick to it. diapedesis
what is the role of basophils?
What about eosinophils?
which one is tightly regulated?
In what 3 ways is it regulated?
what are the 4 markers of eosinophil? test question for sure
which things are part of the prolonged secondary response? Elements?
1IL-5R+FcRg+FcRa+C3R+ (IL-5, IgG, IgA, C3)
Once mast cells loaded- they react via cross linking of Ereceptors. Can provide 2 signals : soluble (IL4) to drive B cells to become IGE.
Can also provide contact with CD40 L to help rpomote B cell growth and differentiation into IgE . This amplifies TH2 response bc of soluble and contact signals.
what is the clinical pathological triad of asthma?
intermittent airway obstruction, chronic bronchial inflammation with eosinophils, and bronchial small muscle cell hyper-reactivity to broncho-contrictors (
why not treat with antihistamines?
Histamine plays little role in airway constriction and anti-histamines have no role in treatment of asthma
how do we treat the following?
1. anaphylaxis?
2. bronchial asthma?
3various allergic diseases
from an evolution standpoint, why do we have type I hypersensitivity
describe the mast cell 3 componenst of the receptor? which part does IgE bind?
