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Hypersensitivity Reactions:. Hypersensitivity reactions : I nflammatory immune responses induced by repeated antigen exposure resulting in host tissue damage. Allergen : is a nonparasitic antigen capable of stimulating hypersensitivity reactions.

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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.
  • An antigen that produces a vigorous immune response in which the immune system fights a threat that is harmless to the body.
types of hypersensitivity
Types of Hypersensitivity:
  • Four groups: according to mechanism of action into
  • Type I (Immediate hypersensitivity).
  • Type II (Cytotoxic hypersensitivity).
  • Type III (Immune complex hypersensitivity).
  • Type IV (Cell-mediated hypersensitivity) (delayed hypersensitivity).
examples of allergen
Examples of Allergen:
  • Exogenous:
  • Animal products: fur and dander, cockroach calyx, wool, dust mite excretion
  • Drugs ( penicillin, sulfonamides)
  • Food : Egg albumen, Corn, legumes (peanuts, soybeans), milk, and seafood.
  • Insect venom.
  • Mold spores.
  • Plant pollens( hay fever)
  • Endogenous: Self antigen.
type i hypersensitivity
Type I Hypersensitivity:
  • Known as allergic or immediate hypersensitivity.
  • The reaction takes 15-30 minutes to appear.
  • It could appear as a delayed response (10-12 hours later).
  • Examples: Eczema, Urticaria , Hay fever, Asthma.

Tow types according to the site of reaction:

  • Localized reaction:

Skin, eye, Nasopharynx, Broncho pulmonary or GIT.

  • Systemic reaction:

In Bloodstream: venom or toxin. Lethal effect.

mast cells
Mast cells
  • Originate from the bone marrow and are scattered in the connective tissues of the body, especially skin, near blood vessels, respiratory system, and digestive tract).
  • very similar to basophils (have granules that contains allergy mediators)
mechanism of type i hypersensitivity
Mechanism of Type I Hypersensitivity:
  • Sensitization phase:
  • Exposure to allergen.
  • Isotype switching to IgE
  • Sensitization of Mast cell by IgE (FcεRI).
  • Effector phase:
  • IgE Cross-linking.
  • Mast cell degranulation and release of vasoactive amines, lipids and cytokines and attraction of eosinophils.
mast cell inflammatory mediators
Mast cell inflammatory mediators:
  • Biogenic amines ( histamines):
  • Bronchiole constriction, and mucus secretion from Goblet cell.
  • Vasoconstriction and capillary endothelial vasodilation ; increased vascular permeability (fluid loss and shock).

Lipid mediators:

  • Leukotriene; similar to histamine effect.
  • PAF(platelet aggregation): micro thrombosis
  • Prostaglandins D2:edema and pain.
  • Cytokines: TNF.
type ii hypersensitivity
Type II Hypersensitivity:
  • Known as Cytotoxic Hypersensitivity.
  • Allergen could be:
  • Endogenous: Cell surface proteins
  • Exogenous: Drugs adsorbed onto cell membrane.

IgG , IgM, Complement, and Cytotoxic cells are involved in this type of inflammation.

  • Sites of occurrence of Type II reactions:
    • On cell surface (Example: RBCs).
    • Within extracellular matrix (Example: Basement membrane).
examples on type ii hypersensitivity
Examples on Type II Hypersensitivity:
  • Alloimmune hemolytic anemia:
    • Erythroblastosis fetalis (maternal IgG X fetal RBCs)
    • Alloimmune hemolytic anemia: Blood transfusion anemia(recipient IgMagainst donor RBCs)
  • Goodpasture’s syndrome (kidneys & lungs).
  • Graves Disease ( Antibodies against TSH receptors) leading to activation.
type iii hypersensitivity
Type III Hypersensitivity:
  • Soluble immune Complex hypersensitivity. (IgG- short peptide or IgG- animal sera).
  • Lead to inflammation at the site of their deposition.
  • Types of Allergen:
  • Exogenous: e.g. animal sera.
  • Endogenous: soluble self antigens.
mechanism of type iii hypersensitivity reaction
Mechanism of type III hypersensitivity reaction:
  • Ag-Ab (IgG) complexes accumulate and deposit (usually in the endothelium) leading to complement activation and neutrophil attraction (C3a, C4a, C5a).

Two types:

  • Localized (Arthus reaction) example: in skin: Intradermal injection of antigen in skin; necrotizing vasculitis.
  • Systemic(Serum sickness): Wide dissemination of immune complexes.
clinical examples
Clinical Examples:
  • Serum sickness disease associated with:

-Some types of food allergy.

-Prophylactic vaccine (animal antisera). Symptoms develop after 7-10 days and is self-limiting after clearance of the antigen.

  • Systemic lupus erythematosus (self antigens).
  • Rheumatoid arthritis (self antigens).
type iv hypersensitivity
TypeIV Hypersensitivity:
  • known as cell mediated (CD4 or CD8)or delayed type hypersensitivity.
  • Antibodies are not involved.
  • The classical example of this hypersensitivity is tuberculin (Mantoux) reaction which peaks 48hours after the injection of antigen (tuberculin).

Three types:

  • Contact dermatitis: toxic sensitizer absorbed through epidermis, bind self proteins & form neoantigen .
  • Delayed type hypersensitivity(DTH): Granulomatous inflammation, not limited to the dermis. Usually due to pathogens e.g. M. tuberculosis.
  • T cell mediated cytotoxicity: caused by CD8T lymphocytes.
clinical example
Clinical example:
  • Tuberculin (Mantoux) test(DTH)
Erythema induratum (Bazin disease): nodules in the legs due to sensitivity to some pathogens e.g. M.tuberculosis