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Hypersensitivity. Department of Microbiology. Important terms. Hypersensitivity reactions are exaggerated antigen-specific immune responses which is harmful to the host. Allergen : The antigens that give rise to immediate hypersensitivity

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Department of Microbiology

Important terms
Important terms

  • Hypersensitivity reactionsare exaggerated antigen-specific immune responses which is harmful to the host.

  • Allergen:The antigens that give rise to immediate hypersensitivity

  • Atopy:The genetic predisposition to synthesize inappropriate levels of IgE specific for external allergens

  • Types of hypersensitivity: As per Coomb and Gel Classification hypersensitivity is of four types (Type I, Type II, Type III and Type IV)

Type i hypersensitivity
Type I Hypersensitivity

  • Mediated by IgE antibodies.

  • Also known as “immediate hypersensitivity "or “Allergic response”.

  • Antigens that induce type I hypersensitivity are also termed as “Allergens”.

Type i hypersensitivity1
Type I Hypersensitivity

  • The IgE antibodies produced against Allergens remain bound to Mast cells.

  • Upon exposure to specific Allergens IgE antibodies induce degranulation of Mast cells.

  • This leads to release of inflammatory mediators like Histamine, Serotonin, Prostaglandins etc.

  • Some common Allergens are Pollen, Dust etc.

  • Example: P-K reaction

Type ii hypersensitivity
Type II Hypersensitivity

  • Type II Hypersensitivity is mediated by antibodies that are produced against the antigenic determinants present on cell surface.

  • As the antigenic determinants are present on cell surface, thus type II reaction is manifested in the form of massive cell destruction.

  • The target cells are lysed by:

    • activation of Complement cascade by the antibody molecules bound on the cell surface.

    • antibody dependent cell mediated cytotoxicity (ADCC).

  • Transfusion reactions and Hemolytic Disease of the Newborn are examples of type II reaction.

  • 1. Surface antigen on target cells

    Target cells: Normal tissue cell, changed or modified self tissue cells

    Common antigen,

    Antigen :

    Blood group antigen,

    Drug antigen,

    Self-antigen modified by physical factors or infection

    Antigen-antibody complex

    2. Antibody, complement and modified self-cell

    Activate complement

    Lyse target cells

    Opsonic phogacytosis

    Destroy target cells


    Mf、NK、 T

    Promote /surpress the target cell funcion

    Stimulating or blocking effect

    Antigen or hapten on cell

    Antibody (IgG, IgM)

    Activate complement


    NK , phagocyte

    Stimulate / block

    Lyse target cell

    Destroy target cell


    Target cell injury

    Change the function ofTarget cell

    Mechanism of Type II hypersensitivity

    3. Common disease of type IIhypersensitivity

    1)Transfusion reaction

    hemolysis : mismatch of ABOblood group, severely destroy RBC

    nonhemolysis : repeat transfusion of allogenic HLA

    drug anaphylactic shock:penicillin

    2) Hemolytic disease of newborn

    Mother Rh- : first baby Rh+(Ab), second baby Rh+,

    fetal RBC destroyed

    3) Autoimmune hemolytic anemia and type II drug reaction

    i. Foreign antigen or hapten

    Penicillin RBC hemolytic anemia

    QuininPlatlet thrombocytopenic purpura

    PyramidoneGranulocyte agranulocytosis

    ii. Self-antigen

    Drug conversion from a hapten to a full antigen

    induce self antibody autoimmune hemolytic anemia

    Type ii hypersensitivity antibody dependent cell mediated cytotoxicity
    Type II HypersensitivityAntibody Dependent Cell Mediated Cytotoxicity

    Animation: Antibodies react with epitopes on the host cell membrane and NK cells bind to the Fc of the antibodies. The NK cells then lyse the cell with pore-forming perforins and cytotoxicgranzymes

    Type ii hypersensitivity antibody mediated cell disfunction
    Type II HypersensitivityAntibody-Mediated Cell Disfunction

    Example: Myasthenia Gravis

    Type iii hypersensitivity
    Type III Hypersensitivity

    • Mediated by immune complexes (Antigen-Antibody complex).

    • During normal immune response only moderate quantity of immune complexes are formed and they are removed efficiently from circulation by phagocytosis.

    • In case of production of large quantities of immune complexes, phagocytes fail to remove all the immune complexes from circulation.

    • Thus, Ag-Ab complexes are deposited in various tissues. They lead to activation of complement components. Activation of complement may leads to destruction of bystander cells.

    Type iii hypersensitivity1
    Type III Hypersensitivity

    • Moreover, under the influence of chemotactic complement components polymorphonuclear cells are recruited at the site.

    • These cells, in their attempt to engulf immune complexes, releases lysozymal enzymes in the tissue and thus cause tissue destruction.

    • Arthus reaction is an example of localized type III hypersensitivity.

    • Serum Sickness is an example of Systemic type III hypersensitivity.

    • Blue Eye: Dogs infected or vaccinated with live canine adenovirus I develops anterior uveitis. This lead to corneal oedema and opacity. The blue eye is considered to be an immune complexes mediated condition.

    Type iii hypersensitivity2
    Type III Hypersensitivity

    • “Immune complex disease”

    • Soluble Ag / IgG or IgM

      • high titers of each required

    • Immune processes involved:

      • classical complement pathway

      • phagocytic cells

    Immunreaktionen der Haut

    Soluble antigen



    Immune complex

    Small molecular soluble

    Immune complex

    intermediate molecular soluble

    Immune complex

    Large molecular insoluble

    Immune complex

    Deposit on the basement of capillaries

    Eliminate by phogacytosis

    Combine and activate complement system

    Basophils and mast cells



    Infiltration of neutrophils

    Blood Clotting Mechanisms

    Release of vasoactive amine

    Phagocytose complex

    Release of vasoactive amine

    Aggregation of platlets

    Release the enzymes in lysosome

    Increase vascular permeability

    Increase vascular permeability



    Tissue injury



    Local or systemic immune complex diseases

    3. common disease of type III hypersensitivity

    1.Local immune complex disease

    Arthusreaction :Experimental local reaction,

    Necrotic vasculitis vasculitis, Ulcer

    Human local reaction: insulin-dependent diabetes mellitus (IDDM)

    2. Acute systemic immune complex disease

    serum sickness 

    Anti-serum Ab+Ag systemic tissue injury ,fever, arthritis, skin rash


    Acute immune complex glomerulonephritis :Streptococcus infection

    3. Chronic immune complex disease


    Rheumatoid arthritis:RF+IgG Deposit on synovial membrane

    Type iv hypersensitivity reaction
    Type IV hypersensitivity reaction

    • Because of delay in onsetof response, type IV hypersensitive reaction is also known as Delayed Type Hypersensitivity (DTH).

    • It approx takes 24 to 48 hours from the time of antigenic stimulation.

    • Unlike Type I, II, and III response (antibody mediated), Type IV reaction is mediated by Cellular immune components.

    Type iv hypersensitivity reaction1
    Type IV hypersensitivity reaction

    • The effector cells of Type IV hypersensitivity response are CD4+ (Th), CD8+ cells and activated macrophages.

      Some common examples of type IV hypersensitivity reaction:

    • Tuberculin test (used for diagnosis of Tuberculosis),

    • Johnin test (used for diagnosis of Johnes disease),

    • Mallein test (used for diagnosis of Glanders),

    • Brucellin test (used for diagnosis of Brucellosis).