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

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

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

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

Here is the comparison table:

S.N.

Character Type I Type II Type III

Type IV

1. Alternative Name Allergic hypersensitivity Cytotoxic hypersensitivity Immune complex hypersensitivity Cell mediated hypersensitivity/ Delayed type of hypersensitivity
2. Principle Antibody mediated degranulation of granulocytes leading to destruction of cells. Antibody mediated destruction of healthy cells. Antigen-antibody complex mediated destruction of cells. T lymphocytes mediated destruction of cells.
3. Primary Mediator IgE IgG/IgM IgG/IgM Specific subsets of CD4+ helper T cells or CD8+ cytotoxic T cells.
4. Other components as mediators Mast cells, Basophils, histamine & other pharmacological agents Complement, Neutrophils Complement, phagocytes and K cells Dendritic cells, macrophages and cytokines
5. Reaction time Immediate or within few hours 5-8 hours 2-8 hours After 24 hours only, mostly 48-72 hours after contact
6. Antigen Free in circulation (Soluble) Fixed on cells Free in circulation ( Soluble) Soluble or cell bound
7. Antigen origin Exogenous Endogenous or exogenous Exogenous or endogenous Exogenous or endogenous
8. Antibody Fixed on mast cells and basophils Free in circulation Free in circulation Not applicable
9. Mechanism 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 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.
10. Complement activation No Yes Yes No
11. Appearance Weal & flare Lysis & necrosis Erythema & edema Erythema & induration
12. Transfer with serum Passive transfer possible with serum Passive transfer Passive transfer Cannot be transferred with serum; but possible with T cells transfer
13. Desensitization Easy but short lived Easy but short lived Easy but short lived Difficult but long lived.
14. Examples 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.

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

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