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Hypersensitivity
Hanzalah Rashid
DPH-4
Definition
Under some circumstances, immune responses produce damaging and
sometimes fatal results, known collectively as hypersensitivity.
Hypersensitivity reactions are classified by the immune mechanism.
● Type I hypersensitivity
● Type II hypersensitivity
● Type III hypersensitivity
● Type IV hypersensitivity
Type I hypersensitivity
Immediate hypersensitivity
It occurs upon the reaction of allergen (an antigen that elicits an allergic
response) with specific IgE antibody.
1. Sensitization phase.
2. Activation phase (Mast Cell Granulation)
3. Effector phase
Clinical tests
● Skin Prick
● Intradermal Injection
● RAST(Radioallergosorbent Test)
● ELISA(enzyme-linked immunosorbent assay)
Treatments
● Avoid exposure
● Desensitization or Modulation of the immunologic response
● Anti-IgE monoclonal antibody (omalizumab)
● Mast cell stabilization.
● Mediator antagonists.
Type II Hypersensitivity
● Antibody mediated
● Production of IgM or IgG antibodies directed to foreign antigens.
● Complement activation, either direct lysis or opsonization;
antibody-dependent cell mediated cytotoxicity via NK cells or
eosinophils; or opsonization by antibody, followed by
phagocytosis by neutrophils and macrophages
1. Type II drug reactions.
● Drugs acting as haptens may become associated with cells or other
components of the body and initiate antibody formation.
● e.g., penicillins, cephalosporins, and quinidine.
● Drug requires approximately 7 to 10 days after the initiation of drug
therapy, at which point, antibody production will be sufficient for cell lysis
and inflammation.
2. Rhesus blood group
● Hemolytic disease of the newborn(HDN).
● During pregnancy of an Rh-negative mother with an Rh-positive child, the
mother may become sensitized to the D antigen of the child’s blood.
Type III Hypersensitivity
● Reactions are mediated by immune complexes of foreign antigen together
with IgG, or occasionally IgM antibodies.
● The presence of the immune complexes results in activation of complement,
including the generation of chemotactic and vasoactive factors.
❖ Arthus reactions
❖ Serum sickness
❖ Hypersensitivity Pneumonitis (farmer’s lung)
Type IV Hypersensitivity
● Delayed-type hypersensitivities.
● Mediated by specific effector T cells.
● Examples of type IV hypersensitivities include the immune response to some
infections (tuberculosis) and contact dermatitis, most often associated with
metals or haptenic chemicals.
❖ Tuberculin skin test
❖ Contact hypersensitivity
❖ Celiac disease

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Hypersensitivity and Types . An Overview

  • 2. Definition Under some circumstances, immune responses produce damaging and sometimes fatal results, known collectively as hypersensitivity. Hypersensitivity reactions are classified by the immune mechanism. ● Type I hypersensitivity ● Type II hypersensitivity ● Type III hypersensitivity ● Type IV hypersensitivity
  • 3. Type I hypersensitivity Immediate hypersensitivity It occurs upon the reaction of allergen (an antigen that elicits an allergic response) with specific IgE antibody. 1. Sensitization phase. 2. Activation phase (Mast Cell Granulation) 3. Effector phase Clinical tests ● Skin Prick ● Intradermal Injection ● RAST(Radioallergosorbent Test) ● ELISA(enzyme-linked immunosorbent assay)
  • 4. Treatments ● Avoid exposure ● Desensitization or Modulation of the immunologic response ● Anti-IgE monoclonal antibody (omalizumab) ● Mast cell stabilization. ● Mediator antagonists.
  • 5. Type II Hypersensitivity ● Antibody mediated ● Production of IgM or IgG antibodies directed to foreign antigens. ● Complement activation, either direct lysis or opsonization; antibody-dependent cell mediated cytotoxicity via NK cells or eosinophils; or opsonization by antibody, followed by phagocytosis by neutrophils and macrophages
  • 6. 1. Type II drug reactions. ● Drugs acting as haptens may become associated with cells or other components of the body and initiate antibody formation. ● e.g., penicillins, cephalosporins, and quinidine. ● Drug requires approximately 7 to 10 days after the initiation of drug therapy, at which point, antibody production will be sufficient for cell lysis and inflammation. 2. Rhesus blood group ● Hemolytic disease of the newborn(HDN). ● During pregnancy of an Rh-negative mother with an Rh-positive child, the mother may become sensitized to the D antigen of the child’s blood.
  • 7. Type III Hypersensitivity ● Reactions are mediated by immune complexes of foreign antigen together with IgG, or occasionally IgM antibodies. ● The presence of the immune complexes results in activation of complement, including the generation of chemotactic and vasoactive factors. ❖ Arthus reactions ❖ Serum sickness ❖ Hypersensitivity Pneumonitis (farmer’s lung)
  • 8. Type IV Hypersensitivity ● Delayed-type hypersensitivities. ● Mediated by specific effector T cells. ● Examples of type IV hypersensitivities include the immune response to some infections (tuberculosis) and contact dermatitis, most often associated with metals or haptenic chemicals. ❖ Tuberculin skin test ❖ Contact hypersensitivity ❖ Celiac disease