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26 Cards in this Set

  • Front
  • Back
What type of hypersensitivity reaction is an allergic response?
Type I.
What Ab is the mediator for an allergic response?
IgE.
Why are IgE's effective in forming an allergic response?
Cross-link with Fcε-R's, which happen to be located on mast cells and basophils.
What was the normal IgE response intended for?
Certain worms, parasites, or anything too large to be phagocytosed - require IgG to intervene and the secondary immune response.
What make basophils and mast cells ideal for creating an immune response?
They have cytoplasmic stores of very potent vasoactive mediators that result in inflammation and tissue damage.
Which component of the allergic response circulate in the plasma?
Basophils.
Which component of the allergic response are embedded in tissue?
Mast cells - mucosa or connective tissue.
What do allergens do to the immune response?
Induce IgE release instead of the normal IgM, IgG, or IgA response.
What is the common component found in many environmental allergens?
Chitin.
Why do allergens cause IgE production instead of a normal response?
Genetic predisposition in MHC II D Loci present allergen peptides that preferentially induce IgE production over IgG by influencing the TLR activated, the T-helper cell activated, and the cytokine milieu during allergen presentation.
Which genes are involved in producing allergies in an individual?
A multiplicity of genes acting in concert.
What can serum IgE levels tell about an individual?
Since they are typically low and undetectable, they give a direct indicator for allergic reactions and the atopic state.
What type of early exposure may incite IgE production and an allergic response?
High levels of exposure to an antigen early in life, coupled with a lack of exposure to antigens that incite a strong Th1 and Th2 responses, may result in allergy.
How would the route of antigen affect allergic response?
Delivery of antigens to the mucsal surface may facilitate an allergic response.
What must accompany every risk factor in order for allergies to develop?
Genetic predisposition.
What is the sequence of an allergic response?
1) Allergen contacts an APC in usually a mucosal surface.
2) Uptake of allergen by an APC via "allergic" TLR's will induce the APC to produce IL-4 instead of IL-12 resulting in a Th2 response. Anything that causes a Th2 bias (IL-4, suppress IL-12) may result in allergic reactions.
3) Allergen is presented by MHC II molecules, and its presentation dictates a dominant, abnormal IgE response.
4) Allergen specific B-cell responds to IL-4.
5) Th2 cytokines are released by APC's and begin to dominate the milieu (IL-4, IL-13).
6) Fcε-R's are upregulated on mast cells and basophils when IgE is promoted, increasing even more IL-4 and IL-13.
7) Presence of IL-4 (Th2 response) will activate the ε germ line transcription in B-cells.
What is "arming" the Fcε-R's on mast cells and basophils?
This is when an allergen specific IgE binds to Fcε-R's without first forming a Ab-Ag complex with the antigen. This occurs during the first processing of allergen to produce IgE.
What will happen when exposure to the same allergen occurs again?
The allergen will bind to the IgE cross-linked to the armed Fcε-R's on mast cells and basophils causing them both to degranulate and release vasoactive and inflammatory mediators.
What is the immediate allergic response?
Within 15 mins of exposure, armed mast cells and basophils degranulate and the classical complement reaction occurs.
What is the late allergic response?
After the immediate response produces copious IL-4 and IL-13, the key cytokine IL-5 is released by Th2 cells and mast cells, together with eotaxin, to recruit eosinophils, resulting in an even greater inflammatory response for a longer period of time by releasing major basic protein. IL-5 increases Fcε-R display even more.
The late phase is completely dependent on Th2 activation.
What do clinical manifestations of allergies depend on?
The site of allergen uptake.
What is allergic rhinitis?
Aero-allergen binds to nasal mucosa, causing an inflammatory reaction and runny nose.
What is the hyperhygiene hypothesis?
Less exposure to vigorous infectious antigens and a more acute exposure later in life may result in a lack of T-regs that regulate IgE production.
What is RAST?
Radiolabeled anti-IgE is added to a well that was seeded with antigen and washed with IgE. If binding occurs, allergen is determined.
What is desensitization treatment?
Rerouting of IgE response to promote Th1 and macrophage destruction of the antigen, or redirect the Th2 response to produce IgG.
What is anti-IgE therapy?
Anti-IgE monoclonal Ab's are engineered to bind to the binding site of circulating IgE's that are specific for the allergen.