Hypersensitivity Reactions:
Definitions:
Hypersensitivity reactions:
inflammatory immune responses induced by repeated
antigen exposure resulting in host tissue damage.
Allergen:
is a nonparasitic antigen capable of stimulating
hypersensitivity reactions.
Types of Hypersensitivity:
Hypersensitivity reactions are divided according to
mechanism of action into four groups:
1-Type I (Immediate hypersensitivity).
2-Type II (Cytotoxic hypersensitivity).
3-Type III (Immune complex hypersensitivity).
4-Type IV (Cell-mediated hypersensitivity).
Types of Allergen:
Exogenous:
1- Animal products.
2- Drugs ( penicillin)
3- Food : Egg albumen, Corn, legumes (peanuts,
soybeans), milk, and seafood.
4- Insect venom.
5- Mold spores.
6- Plant pollens.
Endogenous:
-Self antigen.
Type I Hypersensitivity:
-Commonly known as allergic or immediate hypersensitivity.
-Two types according to affected body sites:
1-Localized reaction:
Skin, eye, Nasopharynx, Bronchopulmonary, and GIT.
2-Systemic reaction:
In Bloodstream.
-The reaction takes 15-30 minutes to appear as
inflammatory response.
-It could appear as a delayed response (10-12 hours later).
-Examples: Eczema, Urticaria , Hay fever, Asthma.
Mechanism of inflammation in Hypersensitivity Type I:
Sensitization phase:
1-Exposure to allergen.
2-Isotype switching (IL-4, IL-13 activity).
3-Sensitization of Mast cell by IgE (FcεRI).
Effector phase:
1-IgE Cross-linking.
2-Mast cell degranulation.
3-Release of vasoactive amines, Lipids, and cytokines.
Type I Hypersensitivity (sensitization phase):
N
Type I Hypersensitivity (Effector phase):
N
Mast cell inflammatory mediators and their action:
1- Biogenic amines ( histamines):
A-Bronchiole constriction, and mucus secretion
from Goblet cell.
B- Endothelial vasodilation ; increased vascular
permeability, and vasoconstriction.
2- Lipid mediators:
A-Leukotriene C4,and D4 ; similar to histamine effect.
B-PAF (platelet aggregation: microthrombosis)
C-Prostaglandins D2 : edema and pain.
3-Cytokines: TNF.
Clinical examples on Type I Hypersensitivity:
1-Localized reaction in Skin:
Urticaria
Eczema
2-Systemic Anaphylaxis: In bloodstream.
Lethal effect.
Type II Hypersensitivity:
-Known as Cytotoxic Hypersensitivity.
-Allergen could be:
1-Endogenous: Cell surface protein.
2-Exogenous: Drug metabolite adsorbed onto cell
membrane.
-Sites of occurrence of Type II reactions:
1-On cell surface (Example: RBCs).
2-Within extracellular matrix (Example: Basement memb).
Mechanism of inflammation in Hypersensitivity Type II:
-IgG , IgM , Complement, and Cytotoxic cells are involved
in this type of inflammation.
Clinical Examples on Type II Hypersensitivity:
1-Immune Hemolytic Anemia:
A-Alloimmune hemolytic anemia.
:Erythroblastosis fetalis
B-Autoimmune hemolytic anemia.
: Blood transfusion anemia.
2-Goodpasture’s syndrome (nephritis).
3-Graves Disease.
Type III Hypersensitivity:
-Immune Complex hypersensitivity.
-Soluble Immune complexes:
(IgG- short peptide-IgG) or (IgG-Animal sera-IgG).
-Two types:
1-Localized in skin: Example: Arthus reaction.
Intradermal injection of antigen in skin; necrotizing
vasculitis .
2-Systemic: Example: Serum sickness disease.
-Types of Allergen:
1-Exogenous.
2-Endogenous: self antigen.
Mechanism of Inflammation in Type III Hypersensitivity:
-Immune complex (IgG), complement, and Neutrophils
are involved.
Clinical Examples on Type III Hypersensitivity:
1-Serum sickness disease that associated with:
-Some types of Food allergy.
-The prophylactic Vaccine.
2-Systemic lupus erythematosis.
3-Rheumatoid arthritis.
Type IV Hypersensitivity:
- known as cell mediated or delayed type hypersensitivity.
- The classical example of this hypersensitivity is
tuberculin (Montoux) reaction which peaks 48 hours
after the injection of antigen (tuberculin).
-Three types:
1-Contact dermatitis: toxic sensitizer or neoantigen.
2-Delayed type hypersensitivity(DTH): Granulomatous inf.
3-T cell mediated cytotoxicity.
Mechanism of inflammation in type IV:
-DTH cell,and toxin or neoantigen are involved.
Clinical example:
Tuberculin test: