Flashcards in Lecture 17: IgE Deck (47)
What kind of hypersensitivity reaction is allergy?
disease following immune response to otherwise innocuous antigen
The ability to transfer reactivity to allergens by means of serum (aka the ability to make IgE)
True or false: allergic reactions have double in the past 10-15 years
What are some clinical manifestations of allergy?
smooth muscle spasm
increased vascular permeability
activation of inflammatory and coagulation cascades
What is a major post translational modification on IgE molecules?
How abundant is IgE in serum?
usually VERY LOW concentrations (it is a cell bound antibody found mainly at host-environmental interfaces)
Where are the binding sites for FcERs? (what cells have them)
mast cells and basophils (and on APCs at much lower levels)
What do basophils and mast cells have in common?
1) cytoplasmic stores of histamine, TNFa, and leukotrienes
2) high affinity IgE FcE receptors
__________ are tissue bound while ________ are mostly in the blood
mast cells; basophils
What are the two toxic mediators in mast cells?
What is the lipid meditator in mast cells?
What distinguishing feature divides the two major subtypes of mast cells?
what enzymes are expressed
MCt = tryptase
MCtc = tryptase and chymase
(but since both have tryptase, tryptase staining is the primary way to identify mast cells)
____ are the primary mast cells of the mucosa while _____ are in the connective tissue like skin
What is one characteristic that many allergens have in common?
What dictates our allergic responses?
our genes (50% of children from 2 atopic parents will be atopic)
Which MHC presents allergens?
2 (D class perhaps promotes IgE production over IgG by influencing the type of TLR activated)
What gene(s) are responsible for allergic reactions?
A multiplicity of them! act in concert
True or false: there is a direct relationship between serum IgE levels, allergic reactions and the atopic state
Almost anything can be an allergen but what heightens the probability that our immune system will mount a response?
What is one big reason for why timing is important in the allergic response?
decreased early exposure to infections in genetically predisposed individuals is associated with insufficient Treg control of IgE
What is the common route of allergens?
How does the body know if it is taking up allergen or actual pathogen? (in other words, what pushes the processing towards the IgE route vs the IgG?)
"allergic" TLRs that induce DC to produce IL-4 instead of IL-12 (Th2 instead of normal Th1)
also, presentation of peptide as well as the nature of it shift it towards the dominant IgE
Allergic responses are dependent on what kind of responses?
What leads to the Th2 response?
presence of IL-4 and lack of IL-12
What 2 cytokines dominate the profile during IgE responses?
IL-4 and IL-13
What is the ONLY receprot that can be occupied without antigen?
(Fc receptor for IgE wants to bind empty IgE - then the cell is armed and ready)
What is required for degranulation of mast cells and basophils?
crosslinking of IgE receptors
What promotes IgE class switching?
upregulation of CD23 on mast cells and basophils that increase their production of IL-4 and 13