Hypersensitivities
Type 1 - IgE mediated (also called anaphylaxis)
Allergy and Asthma fall in this category
People with allergies make IgE (instead of IgG) to common (often environmental) antigens. These antigens are called allergens in this context, but there is no difference between an allergen and an antigen - the difference is in the person and their immunce response.
IgE has the ability to bind to mast cells via the Fc region - see fig. 19.1, page 468 Tortora. (IgG doesn't have this ability.) We say that mast cells have Fc-IgE receptors. Remember that mast cells are filled with "mediators of inflammation." Some of these inflammatory compounds include: histamine, prostaglandins and leukotrienes.
Once coated with IgE - like in fig. 19.1 - the mast cells will release their cargo of inflammatory compounds if the appropriate antigen (allergen) comes around and binds to the IgE on the mast cell surface.
If the allergen reacts only with mast cells in a localized area, a local reaction will occur. This, for instance, is seen with the nose and eye symptoms common in hay fever.
If the allergen is distributed throughout the body a systemic reaction will occur. Such a systemic anaphylaxis or anaphylactic shock may be life threatening - leading to a massive drop in blood pressure and constriction of the airways. This is the type of reaction which is seen in people with bee sting allergies or in people who react after getting a shot of penicillin.
Common allergies are treated with anti-inflammatory agents such as anti-histamines. If the allergen is identified the physician may try hyposensitization therapy (desensitization therapy). In this treatment the patient is repeatedly immunized with small doses of the allergen over a long peroid of time. The idea here is to try to force the immune system to synthesize IgG instead of IgE. If successful, the circulating IgG specific to the allergen will intercept the allergen before the allergen has a chance to bind to the IgE on the surface of mast cells. Since this would block the trigger of the allergic response, these IgG antibodies are often called "blocking antibodies."
Type 2 - IgG or IgM react with antigen on cells and then complement gets activated:
Cells get destroyed (cytotoxic)
Transfusion reactions
Remember that in the ABO blood group system individuals possess antibodies to the antigens they don't possess. (See Table 19.2, pg. 470 Tortora.) Since these antibodies exist in our plasma without prior immunization they are often called natural antibodies.
It is important therefore that patients are transfused with blood that matches their ABO type. If not, the transfused blood will rapidly get destroyed once antibody binds to it and complement gets activated. This can cause a life threatening reaction.
Hemolytic disease of the newborn
This situation occurs when there is an Rh incompatibility between a mother and her fetus. It can occur with Rh negative women who bear children who are Rh positive.
Unlike the ABO system, in the Rh blood group system there are no natural antibodies. That is, if a person is Rh negative she will not "naturally" have antibodies to Rh. An Rh negative person will however make anti-Rh antibodies if she is immunized with red blood cells possessing Rh antigens.
It is common in the last days of pregnancy, as the placenta begins to detach, for some fetal cells to pass into the mother's circulation. This is an immunization. If the fetal cells are Rh(+) and the mother is Rh(-), the mother will begin the process of making anti-Rh antibody (RhoGam; anti-Rh gamma globulin). This is usually not a problem in the first pregnancy if the mother has never been primed with Rh. However with the second such child, the mother will have some antibody from the end of the last pregnancy. These antibodies (IgG) cross the maternal-fetal barrier of the placenta and encounter fetal cells in the placenta. The antibodies react with the Rh antigen on those cells, activate complement and this in turn causes inflammation and some damage to the placenta. The damaged placenta is leaky and fetal cells begin to spill over into the mother. (Remember that this is still early in the second pregnancy. ) This second immunization with fetal cells causes a secondary anti-Rh response. Much more antibody is made and it passes into the child and destroys its red blood cells.
In order to prevent this condition women in such a pregnancy are given RhoGam before and after the birth of their Rh(+) child. The anti-Rh antibody interacts with the Rh(+) cells before the cells react with the mother's B-cells to trigger a primary response. RhoGam is therefore called a blocking antibody.
Thrombocytopenia purpura
Type 3 - IgG or IgM react with soluble antigen, this results in antigen-antibody complexes which activate complement:
Serum sickness
Autoimmune conditions such as Rheumatoid arthritis, Glomerulonephritis after streptococcal infections, Lupus erythmatosis
Type 4 - CD4 T-cells react with antigen. This is Delayed Hypersensitivity.
Tuberculin skin test
In this test a small amount of PPD (Purified Protein Derivative of Mycobacterium tuberculosis) is injected intradermally on the forearm and the reaction is read after 48 hours. 48 hours is a long time, it is a delayed reaction.
What does a positive skin test mean? It means that the person has at some time been infected with M. tuberculosis. The person may or may not be now infected with the organism. There are four possible scenarios if a person in PPD(+):
Poison ivy and Mango rash
Allergic contact dermatitis