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Type 1 Hypersensitivity

immediate type
allergy/ asthma
IgE mediated


Type 2 Hypersensitivity

Cytotoxic Hypersensitivity
Rh mismatch
Ig mediated C activation


Type 3 Hypersensitivity

Immune complex sensitivity
Serum sickness, vasculitis
Ab-Ag complexes


Type 4 Hypersensitivity

Delayed type
TB skin test
hypersensitive pneomonititis
tdth cells


What happens during the sensitization phase of hypersensitivity 1?

There is an antigen (allergen) exposed to body which ends up producing IgE. IgE binds to (mast cells, basophils etc) by attatching to FC3R.


How can labs know there is an allergic reaction taking place based on IgE?

IgE is usually in lower concentrations so when the level is IgE is increased that shows an allergic reaction


What happens during the effector phase of hyper sen 1?

The IgE that is attached to the mast cell binds to the allergen which stimulates cross linking and the mast cell degranulates causing a reaction.
chemical mediators are released


Why is IgE important? Why is it produced?

Genetics and Th cell response: Those that have a th2 response have a greater chance of swtitiching to IgE due to cytokines (IL4, IL5, IL13)
Th1: switch to IgG

Relative Dosage of Allergen
Low Dosage: IgG (will compete for antigen clear up antigen= no no reaction)


What are some of the preformed chemicals stored in the granules of mast cells/basophils/ etc that initiate type 1 hyper

Histamine: vascular permiability/ smooth muscle contraction

Proteases: mucus secretion/ generation of split proucts


What is the main protease enzyme used in type 1?

Trypase: normal levels greater that ng/ bee stng greater than 5; short half life (good for recent reactions)


What are some of the newly formed chemicals that are formed after the class switching of Ig in hypersen. type 1?

Leukotriene: similar to histamine but much more potent; also known as SRS-A;

Cytokines (important in class switching) Ex: IL-4, IL5, IL13 and more


What are the symptoms of an allergic reaction?

Wheal and Flare: red area where inflammation is occuring

Localized atopic: itchy(pritus) and raised (hives) (urticaria)

systemic: vasodilation and shock can occur


What are therapies for allergic reactions?


Desensitization: by giving low amounts of antigens IgG will be activated

Anti-IgE: antibodies prevents binding of IgE to Fc3R


How is type 2 hyper sen brought on?

Antibodies (usuallly IgG or IgM) bind to antigen and promote complement or ADCC which leads to cell lysis


Example of type 2 hyper sens?

Transfusion: giving the wrong blood type

Rh: babies can develop erythroblastosis fetalis (HDN); mother Rh antobodies recognize babies rh as antigen; binds to it activates complements and can lyse babies RBC (RhoGam can help mom not stimulate immune reaction)


What happens during type 3 hyperse?

Ag-Ab reaction occurs but is not taken up by macrophage ; can get localized in kidney; which leads to activation of complements= desruction


What are the steps of type 3?

1. Intro of antigen Ab- ag bind
2. Complement activation; mast neutrophil etc are produced
3. more mediators released
4. destruction of cells in that area


Type 3 Arthus reaction

insect bite causes antibodies to bind to antigen and results in inflammation of skin


type 3 generalized?

excess of antigen; not complete clearacnce; IC circulate and concentrate in one area of body such as kidneys


Serum Sickness type 3

where an individual is given an antiserum raised in another animal.
For example, anti-snake venom produced in horses, when given to people who have been bitten by a venomous snake, the anti-venom neutralizes the toxin.

At this point, ICs are not a problem, however, because the horse antibody is foreign, a human will mount an immune response against the horse antibodies.

If the person gets bitten by a snake again and is subsequently given horse anti-venom, the anti-horse antibodies (Ab) will complex with the horse anti-serum (in this case, the Ag).
The resulting Ag-Ab complexes (e.g. IC) will clump together and result in serious inflammation


Vasculitis type 3

Complement activation, especially through the production of the inflammatory split products of C5a (and C3a to a lessor extent) recruit inflammatory cells (e.g. neutrophils, etc) to the area. Together, these result in tissue damage where the ICs are located.


What is the importance of DTH cells

release of th1 cytokines to cause inflammation
Good: kills infectious microbes
Bad: if not controlled inflammation can lead to damage


type 4 and tb?

small amount of m. tuber protein injected. if previously exposed memory Tdth cells will recognize it and produce inflammation response