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

Image Source: Pinterest.

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.