Allergy and Hypersensitivity

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Hypersensitivity is an immune response results in exaggerated reactions harmful to the host. Hypersensitivity is classified into four types:

  1. Type I hypersensitivity
  2. Type II hypersensitivity
  3. Type III hypersensitivity
  4. Type IV hypersensitivity

Type I Hypersensitivity

  • Ig E-mediated hypersensitivity.
  • Immediate reaction.
  • Allergen such as foods, pollen, dust mice and insect venom can induced the formation of IgE in the body.
  • In first exposure, Ig E antibodies bind to the mast cells or basophil via Fc region of Ig E. It is called sensitization.
  • In re-exposure to the allergen, cross-linkage of the membrane bound Ig E happen. It causes the degranulation and releasing of chemical mediators such as histamine, prostaglandins and kininogen which induce vasodilation, smooth muscle contraction, edema, mucus secretion, vascular permeability, bronchial spasm etc.
  • The Type I hypersensitivity can be either atophy or anaphylaxis.
  • Atophy is the local form. It is mainly due to predisposition of family genetic. The example of allergen are pollens, duct mite, milk, seafood etc.
  • Anaphylaxis is the systemic form where the exposure of the allergen to a person who previously sensitized before. The example of allergen is penicillin.

allergy, hypersensitivity, immunology, biology

Allergy (Hypersensitivity Type I)
Image credit: Microsoft

Type II Hypersensitivity

  • Antibody-mediated cytotoxic reaction (Ig G or Ig M).
  • Antibodies find to the antigen at the surface of membrane and causes cell lysis.
  • Cell lysis is due to the formation of membrane attack complex by activation of complement.
  • Opsonization occurs where the phagocytosis is enhanced by opsonin.
  • C3a and C5a induce neutrophil chemotaxis.
  • The most common example are ABO blood group and rhesus  incompatibilities.
  • In Rhesus incompatibility of newborn, baby who inherit rhesus antigen from the father will induce immunization against rhesus antigen in his rhesus negative mother. During birth, fetal blood cells and mother blood cells get contact and induce sensitization. Maternal anti-rhesus antibodies remain in the mother body. In the subsequent pregnancy, the anti-rhesus antibodies pass through placenta to fetal and cause hemolytic to rhesus positive fetal.

Type III Hypersensitivity

  • Immune-complex mediated reaction.
  • Immune complexes are formed when Ig G or Ig M bind with surface membrane of cells.
  • Immune complexes can deposit at the basement membranes of tissues can cause tissue destruction. This is called Arthus reaction.
  • It also induces production of anaphytoxins (C3a and C5a) and increases vascular permeability.
  • Neutrophils are attracted by immune complex. It induces releasing of lysozyme enzyme and damage the tissue.
  • Microthrombi occur which lead to ischemia.
  • Example: Systemic Lupus Erythematosus (SLE).

Type IV Hypersensitivity

  • Delayed type hypersensitivity.
  • Haptens bind to carrier protein in the skin.
  • Hapten-carrier protein complexes are bound by antigen presenting cells and cause activation of T cells in lymph node. It is so called sensitization.
  • If the person is re exposed to the hapten, the sensitized T cells migrate to skin where they proliferate. They secrete cytokines IFN-? and TNF which cause edema and inflammation.
  • Example factors: Poison oak, compound containing nickel or chrome.

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