Page 113 - Color_Atlas_of_Physiology_5th_Ed._-_A._Despopoulos_2003

Hypersensitivity Reactions (Allergies) by the complement system. This leads to the
development of serum sickness (! B), the main
Allergy is a specific, exaggerated immune re- symptoms of which are joint pain and fever.
sponse to a (usually harmless) foreign sub- Type IV reactions are mainly mediated by T H1
stance or antigen (! p. 94ff.). Allergens are an- cells, T C cells, and macrophages. Since symp-
tigens that induce allergies. Small molecules toms peak 2 to 4 days after antigen contact,
conjugated to endogenous proteins can also this is called delayed type hypersensitivity.
have antigenic effects. In this case, they are re- The main triggers are mycobacteria (e.g. Tbc),
ferred to as incomplete antigens or haptens. other foreign proteins, and haptens, such as
The heightened immune response to second- medications and plant substances, such as poi-
ary antigen contact (! p. 94ff.) normally has a son ivy. Primary transplant rejection is also a
protective effect. In allergies, however, the first type IV hypersensitivity reaction. Contact der-
contact with an antigen induces sensitization matitis is also a type IV reaction caused by
(allergization), and subsequent exposure leads various haptens (e.g., nickel in jewelry).
to the destruction of healthy cells and intact
tissue. This can also result in damage to endog- Blood Groups
enous proteins and autoantibody production.
Inflammatory reactions are the main causes of A person’s blood group is determined by the type of
antigen (certain glycolipids) present on the red blood
damage. cells (RBCs). In the AB0 system, the antigens are A
Types of hypersensitivity reactions: Type I
Blood reactions are common. On first contact, the al- and B (! C). In blood type A, antigen A (on RBC) and
anti-B antibody (in serum) are present; in type B, B
4 lergen internalized by B cells is presented to and anti-A are present; in type AB, A and B are pres-
ent, no antibody; in type 0 (zero), no antigen but
T H2 cells. The B cell then proliferates and differ-
entiates into plasma cells (see p. 98), which re- anti-A and anti-B are present.
When giving a blood transfusion, it is important
lease immunoglobulin E (IgE). The Fc fragment that the blood groups of donor and recipient match,
of IgE binds to mast cells and basophils. On sub- i.e. that the RBCs of the donor (e.g. A) do not come in
sequent contact, the antigens bind to the al- contact with the respective antibodies (e.g. anti-A)
ready available IgE-linked mast cells (! A). in the recipient. If the donor’s blood is the wrong
Due to the rapid release of mostly vasoactive type, agglutination (cross-linking by IgM) and
mediators of inflammation such as histamine, hemolysis (bursting) of the donor’s RBCs will occur
leukotrienes and platelet-activating factor (! C1). Donor and recipient blood types must there-
(PAF), an immediate reaction (anaphylaxis) oc- fore be determined and cross-matched (! C2) prior
curs within seconds or minutes: immediate to a blood transfusion. Since AB0 antibodies belong
to the IgM class, they usually do not cross the
type hypersensitivity. This is the mechanism placenta.
by which allergens breathed into the lungs In the Rh system, antibodies against rhesus an-
trigger hay fever and asthma attacks. The va- tigens (C, D, E) on RBCs do not develop unless prior
sodilatory effect of a generalized type I reac- sensitization has occurred. D is by far the most an-
tion can lead to anaphylactic shock (see p. 218). tigenic. A person is Rh-positive (Rh+) when D is pres-
In type II reactions, the immune system ent on their RBCs (most people), and Rh-negative
–
mainly attacks cells with antigenic properties. (Rh ) when D is absent. Anti-D antibodies belong to
This can be attributable to the transfusion of the IgG class of immunoglobulins, which are capable
of crossing the placenta (! p. 93 D). Rh individuals
–
the erythrocytes of the wrong blood group or can form anti-Rh+ (= anti-D) antibodies, e.g., after
the binding of haptens (e.g., medications) to sensitization by a mismatched blood transfusion or
endogenous cells. The binding of haptens to of an Rh mother by an Rh+ fetus. Subsequent expo-
–
platelets can, for example, result in throm- sure to the mismatched blood leads to a severe an-
bocytopenia. tigen-antibody reaction characterized by intravascu-
lar agglutination and hemolysis (! D).
Type III reactions are caused by antigen-antibody
complexes. If more antigen than antibody is availa-
ble, soluble antigen-antibody complexes circulate in
blood for a long time (! B) and settle mainly in the
100 capillaries, making the capillary wall subject to attack
Despopoulos, Color Atlas of Physiology © 2003 Thieme
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