Hypersensitivity Reaction Type1, Type2, Type3 And Type4

Hypersensitivity Overview

Hypersensitivity refers to a condition in which immune response results in excessive reaction leading to tissue damage, disease, or even death in the sensitized host. Hypersensitivity occurs in individuals who had previous contact with the antigen. The underlying contact sharpens the safe framework and the ensuing contact with a similar antigen causes extreme touchiness. A hypersensitivity reaction is classified into four major types.

Classification Of Hype Hypersensitivity 

  • Hypersensitivity reactions are classified into four major types, Type 1, Type 2, Type 3, and Type 4.

1. Type-1 Reaction:

Anaphylaxis is the classical example of a type 1 hypersensitivity reaction. It is an IgE mediated reaction. Type 1 reaction occurs in two forms- the acute potentially fatal, a systemic form called anaphylaxis, and the recurrent non-fatal localized from called atopy.

Mechanism of Anaphylaxis

Anaphylaxis occurs when a sensitized individual comes in contact with a shocking dose of antigen. An interval of 2-3 weeks is required between sensitizing and shocking dose, during which cytotoxic antibody IgE produced against the antigen attaches to surface receptors of mast cells and basophils.
IgE molecules bind to these receptors by their Fc end.

Once sensitized, the individual remains so for a long period. When a shocking does of the same or immunologically related antigen is given, the antigen combines with cell-bound IgE antibody on mast cell rapidly. The antigen-antibody bond complex stimulates mast cell and basophils to release mediators that cause clinical manifestations of anaphylaxis.

Chemical Mediators

The chemical mediators are of two types of primary mediators which are the performed contents of mast cell and basophil granules and the secondary mediators which are newly formed upon incitement of pole cells, basophils, and different leucocytes

2. Type-2

The cytotoxic reaction is mediated by IgG antibodies directed against antigens on the surface of cells resulting in cell damage. Antibodies bind to an antigen on the cell surface and cause phagocytosis, cytotoxicity by natural killer cells and lysis through activation of the complement system. Examples include autoimmune anemias, hemolytic disease of the newborn, and drug reactions.

3. Type-3:

It is characterized by the deposition of antigen and antibody complexes in tissues, activation of complement, and infiltration of polymorphonuclear leucocyte leading to tissue damage. Two typical type 3 reactions include Arthus reaction due to relative excess and serum sickness because of relative antigen excess.

ARTHUS REACTION

Arthus observed that with repeated subcutaneous injection of normal horse serum into rabbits, the initial injections were without any local effect but with later injection, intense local edema and hemorrhagic necrosis develop. This type of reaction is called the Arthus reaction. The Arthus reaction can be passively transferred with sera containing a high titer of antibodies.

SERUM SICKNESS

It is a systemic form of type 3 hypersensitivity reaction. It appears following a single injection of a high concentration of foreign serum. Antibodies to foreign serum reach high enough titers by 7-12 days but still, some excess antigen remains in the circulating blood.

Insusceptible buildings get the store on the endothelial covering of veins in different pieces of the body, causing incendiary penetration. Massive compliment activation and fixation by antigen-antibody complexes lead to a fall in complement concentration.

Serum sickness differs from other hypersensitivity reactions in that a single reaction serves both as the sensitizing and shocking dose. Immune complexes damage the tissue in the same way as that in Arthus reaction. Some important immune complex diseases are posted streptococcal glomerulonephritis, endocarditis, and dengue hemorrhagic fever.

4. Type-4

The reaction is mediated by sensitized T-lymphocyte which on contact with specific antigen, release lymphokines that cause biological effects on macrophages, leucocyte, and tissue cells. Type 4 hypersensitivity occurs within 48-72 hours of antigen challenge.


As it is not antibody-mediated, it cannot be passively transferred by lymphocytes or the transfer factor. Two types of delayed hypersensitivity reactions are well recognized, the tuberculin type and the contact dermatitis type.

Tuberculin Type

When a small dose of tuberculin is injected intradermally in an individual sensitized to tuberculoproten by prior injection or immunization, erythema and swelling occur at the site of injection within 48-72 hours. The injection site is infiltrated by a large number of lymphocyte and about  10-12% macrophages. In an unsensitised individual, the tuberculin injection provokes no response.

The tuberculin test is a useful indicator of delayed hypersensitivity to the bacillus. The positive tuberculin test does not indicate present infection but implies that the person has been infected or immunized by the microorganism in the past. Cell-mediated hypersensitivity reaction develops in much information with bacteria, fungi, and parasites

Dermatitis Type

Delayed hypersensitivity may sometimes develop as a result of skin contact with a range of sensitizing materials metals such as penicillin or other antibiotics in ointments, simple chemicals like hair dyes, picryl chloride, cosmetics, and soaps. These substances can act as haptens. After absorption through the skin, these molecules combine with skin protein to become antigenic. Cell-mediated immunity is induced in the skin. The dermis is infiltrated predominantly by lymphocyte and few macrophages.

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