Last Updated on January 9, 2020 by Sagar Aryal

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