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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
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).
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 (
FcRI). Effector phase: 1-IgE Cross-linking. 2-Mast cell
degranulation. 3-Release of vasoactive amines, Lipids, and
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 C 4,and D 4 ; similar to histamine effect. B-PAF
(platelet aggregation: microthrombosis) C-Prostaglandins D 2 :
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
Clinical Examples on Type II Hypersensitivity: 1-Immune
Hemolytic Anemia: A-Alloimmune hemolytic anemia. :Erythroblastosis
fetalis B-Autoimmune hemolytic anemia. : Blood transfusion anemia.
2-Goodpastures 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.
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
Mechanism of inflammation in type IV: -DTH cell,and toxin or
neoantigen are involved.