(From Dr. Cain’s Lecture, 20 Sept 2000, by Brian Buschman)
Return to Semester Three Goodies
Return to The Unofficial Ross Page
Anaphylactic type hypersensitivity occurs when Ag binds IgE on mast cells and causes release of mediators. The initial exposure to an Ag causes IgE production but the second causes Ag cross linking with the IgE on the mast cells and induces the reaction.
Mediators of type I hypersensitivity include histamine, SRS-A (leukotriene), ECF-A (eosinophil chemotactic factor of anaphylaxis), seretonin, prostaglandins and thromboxane.
The sensitization occurs because APCs take Ag and present them to TH2 cells which secrete IL-4 and IL-10 in the presence of IFN-g and cause the b-cells to make IgE. TH2 cells play a role in humoral immunity where TH1 cells function in cell mediated immunity.
TH cells stem from a common TH0 cell and based on environmental factors change to become TH1 and TH2 cells. If exposed to IL-12 the TH0 cell will become a TH1 cell that releases IL-2 and IFN-g to cause the b-cells to make IgG2. It does not have a primary role in Ig production but mediated type IV hypersensitivity reactions. If exposed to IL-4 and IL-13 it becomes a TH2 cell that releases IL-4 and IL-13 to cause the b-cell to become an IgG1 producing cell which is quickly converted into an IgE producing cell hence mediating hypersensitivity.
Atopy is the fancy word for allergy which is caused by excessive IgE to certain antigens that are things like mold, dust, pollen, peanuts and similar products. The IgE mediates it and if serum from an atopic patient is put into a non-atopic patient the non-atopic patient will have a reaction to the allergen.
Atopy can be tested for by the skin test that leads to local inflammatory reaction and corresponds to a RAST test indicating elevated IgE levels. Bronchioconstriction, inflammation and increased mucus production is often seen.
There are two forms of desensitization.
1) Acute desensitization is when you administer the Ag to the patient at 15 min intervals to build up a tolerance. This tolerance is short lived (days) and allows this method to be useful for administering a drug on the short term when the patient is allergic to the drug.
2) Chronic desensitization involves the administration of the Ag at week long intervals. This causes formation of IgG that binds Ag and prevents it from reaching the IgE to mediate the reaction. This is what’s up with allergy shots.
In type II reaction IgG binds to Ags which then bind to effectors cells and activates the complement pathway to attack the membrane through the normal mechanisms of the compliment system.
Type II hypersensitivity mediates RBO incompatibility, anti-Rh, hemolytic anemias, myasthenia gravis and Good pasture’s syndrome.
Immune complexs are normall formed in infection and the complexes are removed. Sometimes the complexes are not removed but are deposited in tissues like the kidney. It may be a self-Ag in the case of autoimmune disease. The complexes can be seen with immunoflorescence.
The problem is that the residual complexes are attacked by acute-phase reactants and macrophages, basophils and platelets. The compliment system may also be activated.
The injection of serum or certain drugs (iv- penicillin can cause immune complex formation. The complexes induce fever which causes al sorts of problems.
An arthus reaction is the redness and heat felt at the site of a skin irritation. It is not puffed out and swollen the way poison ivy is (type IV) but is a flat, red, hot rash.
Examples include:
1) Glomerulonephritis which makes immune complexes that are deposited in the glomeruli. It causes inflammation and problems.
2) Rheumatoid arthritis has IgM and IgG that binds the Fc region of IgG. This causes immune complexes that are deposited in joints and cause problems.
3) SLE has Abs to DNA and nucli. They form complexes that activate compliment and the C5a attracts neutrophils to kill the tissues.
Delayed hypersensitivity is mediated by TH1 cells. It’s mechanisms cell mediated rather then humoral. In other words NO Igs.
A contact sensitivity like with poison ivy.
The individual who has been previously exposed to TB will test positive to the PPT skin test after a day or two.
If any form of type IV reaction becomes chronic a granulomas will develop.
Return to Semester Three Goodies
Return to The Unofficial Ross Page