Hypersensitivity Type I, II, III and IV- Summary in table form

Hypersensitivity Type I, II, III and IV in one table

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Here is the comparison table:

Alternative Name

Type I Type II Type III Type IV
Allergic hypersensitivity Cytotoxic hypersensitivity Immune complex hypersensitivity Cell-mediated hypersensitivity/ Delayed type of hypersensitivity

Principle

Type I Type II Type III Type IV
Antibody-mediated degranulation of granulocytes leading to the destruction of cells. Antibody-mediated destruction of healthy cells. Antigen-antibody complex-mediated destruction of cells. T lymphocytes mediated the destruction of cells.

Primary Mediator

Type I Type II Type III Type IV
IgE IgG/IgM IgG/IgM Specific subsets of CD4+ helper T cells or CD8+ cytotoxic T cells.

Other components as mediators

Type I Type II Type III Type IV
Mast cells, Basophils, histamine & other pharmacological agents Complement, Neutrophils Complement, phagocytes and K cells Dendritic cells, macrophages, and cytokines

Reaction time

Type I Type II Type III Type IV
Immediate or within a few hours 5-8 hours 2-8 hours After 24 hours only, mostly 48-72 hours after contact

Antigen

Type I Type II Type III Type IV
Free in circulation (Soluble) Fixed on cells Free in circulation ( Soluble) Soluble or cell-bound

Antigen origin

Type I Type II Type III Type IV
Exogenous Endogenous or exogenous Exogenous or endogenous Exogenous or endogenous

Antibody

Type I Type II Type III Type IV
Fixed on mast cells and basophils Free in circulation Free in circulation Not applicable

Mechanism

Type I Type II Type III Type IV
Allergen-specific IgE antibodies bind to mast cells via their Fc receptor. When the specific allergen binds to the IgE, cross-linking of IgE induces degranulation of mast cells. IgG or IgM antibody binds to a cellular antigen, leading to complement activation and cell lysis. IgG can also mediate ADCC with cytotoxic T cells, natural killer cells, macrophages, and neutrophils. Antigen-antibody complexes are deposited in tissues. Complement activation provides inflammatory mediators and recruits neutrophils. Enzymes released from neutrophils damage tissue. Th2 cells secrete cytokines, which activate macrophages and cytotoxic T cells.

Complement activation

Type I Type II Type III Type IV
No Yes Yes No

Appearance

Type I Type II Type III Type IV
Weal & flare Lysis & necrosis Erythema & edema Erythema & induration

Transfer with serum

Type I Type II Type III Type IV
Passive transfer possible with serum Passive transfer Passive transfer Cannot be transferred with serum; but possible with T cells transfer

Desensitization

Type I Type II Type III Type IV
Easy but short-lived Easy but short-lived Easy but short-lived Difficult but long-lived.

Examples

Type I Type II Type III Type IV
Asthma, Rhinitis, Atopic eczema, Bee sting reaction Rhesus incompatibility (Rh hemolytic disease), Transfusion Reactions, Cell Destruction due to autoantigens, Drug-Induced Hemolytic Anemia Glomerulonephritis, Systemic Lupus Erythematosus, Farmer’s lung arthritis, Vasculitis The tuberculin reaction, Granuloma formation, Allergic contact dermatitis, Type-1 diabetes

References

  1. https://courses.lumenlearning.com/microbiology/chapter/hypersensitivities/
  2. http://www.biologydiscussion.com/immunology/4-main-types-of-hypersensitivity-immunology/61851
  3. https://www.slideshare.net/drsomeshwaranamsana/hypersensitivity-reactions-dr-somesh-microbiology
  4. http://www.yourarticlelibrary.com/immunology/type-iii-hypersensitivity-and-its-mechanism-human-immunology/28081
  5. Lydyard, P.M., Whelan,A.,& Fanger,M.W. (2005).Immunology (2 ed.).London: BIOS Scientific Publishers.
  6. Owen, J. A., Punt, J., & Stranford, S. A. (2013). Kuby Immunology (7 ed.). New York: W.H. Freeman and Company.

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