Hypersensitivity

HYPERSENSITIVITY
REACTIONS
Engole Bernard
Introduction
• An immune response inappropriate to an antigen
• Antigens that cause hypersensitivity are termed as
allergens
Hypersensitivity Reactions
• Develop in the course of Humoral and Cell mediated
immunity
• Anaphylactic reaction –Initiated by Ab or Ag-Ab complex
–Referred to as immediate type hypersensitivity reaction –
Symptoms manifest within mins/hrs recepient encounters
the Ag
• Delayed type Hypersensitivity(DTH)-Delay of symptoms
Classifications
• Type I (Immediate) Hypersensitivity

• Type II (cytotoxic) hypersensitivity
• Type III (immune complex mediated)
hypersensitivity-Humoral Branch
• Type IV (delayed) hypersensitivity-Depends on
activation of T cells
Type I:Anaphylactic reactions
• Mediated by IgE antibodies
• IgE binds on mast cells and basophils
• A later exposure to the same allergen The IgE antibodies trigger
the mast cells and basophils to release pharmacologically active
agents causing symptoms of anaphylaxis
• pharmacologically active mediators released from granules act
on surrounding tissue causing vasodilation and smooth muscle
contraction
• Reactions are rapid,occurs within mins after reexposure to the
antigen
Type I (Immediate) Hypersensitivity
Treatment
Avoidance of known allergens
Localized reactions use OTC antihistamines and
decongestants.
Asthma uses combination – antihistamines, bronchodilators
and corticosteroids.
Systemic use epinephrine
In-Vivo Tests - Skin tests
• Testing
• Small amount of allergen injected into skin
• Look for wheal formation of 3mm or greater in diameter
• Simple, inexpensive, can screen for multiple allergens.
• Stop anti-histamines 24-72 hours before test.
• Danger of systemic reaction
• Not for children under 3
Type I (Immediate) Hypersensitivity
The reactions shown here demonstrate allergic response.
Type II: Cytolytic or cytotoxic reaction
• Occurs when IgM or IgG antibodies bind to antigen on the surface of
the cells and activate complement cascade
• It ends with the destruction of the cells
 Triggered by antigens found on cell surfaces
Three Examples of Type II Hypersensitivity
Reactions
• Transfusion Reactions
– Occurs with ABO blood antigen groups
– Complement mediated lysis
• Drug Induced Hemolytic Anemia
– Occurs when an antibiotic forms a complex with red blood cell
membrane protein (similar to hapten carrier complex)
– Induces formation of antibodies
– Complement
• Hemolytic Disease of the Newborn
Type II: Cytolytic or cytotoxic reaction
Transfusion reactions
 Hundreds of different antigens expressed on RBCs
 Antibodies can be produced naturally or through exposure,
transfusion or pregnancy most common
Most well known example due to ABO incompatibility.
 Individuals form potent antibodies against ABO antigens not present
on their red blood cells.
 Group O individuals have anti-A and if transfused with group A
blood will have an immediate, and possibly fatal, reaction
Other blood groups may cause delayed reaction or acute
reactions.
Type II (Cytotoxic) Hypersensitivity
Hemolytic disease of the fetus and newborn
 Mother exposed to blood group antigens due to previous pregnancy with

antigen positive child or transfusion.
 Antibody must be IgG
 Crosses placenta and coats fetal RBCs, destruction of RBCs causes
increased bilirubin and anemia.
 If first pregnancy is first exposure infant usually not affected.
 Subsequent pregnancies have increased risk and the disease ranges from
mild to fatal.
 All pregnant women are screened for blood group antibodies.
Hemolytic disease of the fetus and
newborn
• Occurs via maternal IgG Ab’s crossing the placenta
• In severe cases causes erythroblastosis fetalis
– Most commonly develops in Rh- mother with Rh+ fetus
– Exposure to Rh+ fetal RBC’s stimualtes prod of memory/plasma
– Activation of memory cells in subsequent pregnancy stim IgG Ab’s which
can cross the placenta
– mild-severe hemolytic anemia ensues along with bilirubin which affects
the brain/CNS
• Treatment centers on anti-Rh antibodies (Rhogam)
• Mothers can be tested for anti-Rh antibodies to check for a rise in titre
• Isolated fetal RBC’s can be checked for anti-Rh IgG w/ Coombs test
Drug induced hemolytic anaemia
• Certain antibiotics (eg Penicillin,cephalosporin ,streptomycin)

• Can adsorb nonspecifically to proteins on RBC forming a complex
similar to hapten carrier complex
• In some patients such drug protein complexes induces the formation of
antibodies which then bind to the adsorbed drug on RBC inducing
complement mediated hemolysis and progressive anemia
• When the drug is withdrawn the hemolytic anemia disappears
Type III Hypersensitivity Reactions
• Similar to Type II, IgG or IgM involved and destruction is
complement mediated.
• Difference is that antigen is SOLUBLE.
• Soluble antigen and antibody combine to form complexes.
• Usually complexes cause no symptoms, quickly disappear from the
circulation.
• Size of complexes produced is important in determining whether they
will be eliminated quickly from the body or retained long enough to
cause damage.
• In some individuals the immune complexes persist in circulation
causing clinical symptoms, some of them serious.
Type III (immune complex mediated)
Hypersensitivity
Type IV/Delayed type Hypersensitivity
reaction
• Results from reactions involving T lymphocytes.
• Characteristics of this phenomenon are:
– Delayed, taking 12 hours to develop.
– Causes accumulation of lymphs and macrophages.
– Reaction is not mediated by histamine.
– Antibodies are not involved in the reaction
Type IV (delayed) Hypersensitivity
Positive TB Test
Type IV (delayed) Hypersensitivity
• Contact dermatitis due to contact with chemicals
– Poison ivy, oak and sumac
– Nickel, rubber, formaldehyde, hair dyes, comsetics
– Latex allergies
– Function as haptens
– Causes erythema, swelling and formation of papules
Poison Ivy contact
dermatitis
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Hypersensitivity

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HYPERSENSITIVITY

• Type I (Immediate) Hypersensitivity

 Mother exposed to blood group antigens due to previous pregnancy with

• Certain antibiotics (eg Penicillin,cephalosporin ,streptomycin)

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