1) What makes some antigens capable of these responses?
2) What are the three key players in Hypersensitivity I?
3) What type of Allergens that cause Type I hypersensitivity?
4) Where re IgE found when they are relased?
5) Explain how IgE leads to degranulation of Mast cells or other cell and ultimately the formation
of the inflammatory response.
6) Early response is caused by degranulation of mast cells, explain what are the things that are
released by the cells? What response is this called?
7) What happen in secondary response?
8) Why is this initial response important?
9) Late response: what happen in here? What is needed for this to occur?
10) Explain the steps of HS 1 response?
11) Anaphylactic shock: what is it causes by? What are the key determinants (cytokines) of this
response? What drug is used to inhibit this response and why?
12) What are some ways of treating A shock?
13)What are the two theories of how hyposensitivity works?
14)What are the key players of HS II? ( cell and proteins etc)
15) How is complement fixation involved in HS II? NK induced apoptosis? What decide to kill a
16) Erythroblastosis fetalis: what is it? Caused by? How it causes damage?
17) What happens when a first child RH+ is form and mother is RH?? Why is child safe?
18) What happens if seconds child is born with RH+ now to the same mom?
19) What are the preventive measures you can take for the above problem?
20)Key mediators of HS III?
21)Immune complexes: what are they? How are they normally treated?
22)Immune complexes: what is problem associated with them? How is this problem dealth with
that creates more problem? What part of the body does it damage?
23) What is serum sickness?
24) HS IV: key players? Generally causes by extracellular or intracellular stuff?
25)What is the sensitization phases?
26)What happens in reexposure? Name a disease that uses this mechanism.
27)What is the hygiene hypothesis. Hyppersensitivity:
1) Motifs that resemble PAMPs, Many have protease activity which disrupts epithelial cell
junctions, increasing its exposure to immune cells.
2) IgE and Mast cells and the allergens.
3) Generally proteins or glycoproteins. These elicit IgE antibodies, which are otherwise involved in
immune responses against parasitic infections
4) Binds Fc receptors (FcεR) on eosinophils, mast cells, and basophils. Usually involved in killing
worms ( they bind to it and then these cells then come in)
5) IgE binds the FcERI receptor ( which are very high affinity IgE receptors) that is expressed on
eosinophils, basophils, and mast cells. It is comprised of an α chain that IgE actually binds to,
and a β strand and two γ strands that contain ITAMS. when crosslinking of antibodies on Fc
receptors binding the same antigen happens, ITAMs phosphorylate adaptor proteins which leads
to activation of downstream signalling. In this case, it causes degranulation and release or
synthesis of numerous mediators involved in inflammation Similar to what we have discussed in
6) Granule exocytosis which contain vasoactive amines (histamine) and protease ( which degrade
blood vessel basement) and Chemotactic factors ( attraction of other cells). Effectors in
granules are considered primary as they are preformed and act immediately
7) Lipid mediators (prostaglandin), which are for smooth muscles contractions and permeability,
and Cytokines, which are for IgE production, signal, systemic anaphylaxis, and bring in more
cells. These are considered secondary – they are synthesized or are released from the breakdown
of membrane phospholipids following degranulation
8) These mediators are recruiting immune cells and making it easier for them to leave the blood into
tissues, as well as mucous secretion to catch more pathogens during real infection (bad during
9) Mediated primarily by eosinophil’s and neutrophils recruited by chemokine’s and cytokines that
increase endothelial cell adhesion. These degranulation, causing further damage
10)B cell First expo