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Comparison of hypersensitivity types

Often mentioned
Type Alternative names Mediators Description
disorders

Fast response which occurs in minutes,

Atopy
rather than multiple hours or days. Free
Anaphylaxis antigens cross link the IgE on mast cells
I Allergy (immediate) IgE and basophils which causes a release of
Asthma
Churg-Strauss vasoactive biomolecules. Testing can be
Syndrome done via skin test for specific IgE.[2]

Autoimmune
hemolytic anemia
Rheumatic heart
disease
Thrombocytopenia Antibody (IgM or IgG) binds to antigen on
Erythroblastosis a target cell, which is actually a host cell
Cytotoxic, antibody- fetalis IgM or IgG that is perceived by the immune system
II Complement as foreign, leading to cellular destruction
dependent Goodpasture's
syndrome MAC via the MAC. Testing includes both the
Graves' disease direct and indirect Coombs test.[3]
*see type V
explanation below
Myasthenia gravis
*see type V
explanation below

Serum sickness
Rheumatoid
arthritis
Arthus reaction
Post streptococcal
glomerulonephritis Antibody (IgG) binds to soluble antigen,
Membranous IgG forming a circulating immune complex.
Immune complex nephropathy This is often deposited in the vessel walls
III Complement
disease of the joints and kidney, initiating a local
Reactive arthritis
Neutrophils
Lupus nephritis inflammatory reaction.[4]
Systemic lupus
erythematosus
Extrinsic allergic
alveolitis
(hypersensitivity
pneumonitis)

IV Delayed-type T helper cells (specifically Th1 cells) are

hypersensitivity,[2][3] Contact T-cells activated by an antigen presenting cell.
cell-mediated dermatitis, When the antigen is presented again in
immune memory including Urushiol- the future, the memory Th1 cells will
response, antibody- induced contact activate macrophages and cause an
independent dermatitis (poison inflammatory response. This ultimately
ivy rash). can lead to tissue damage.[6]
Mantoux test
Chronic transplant
rejection
Multiple
sclerosis[5]
Coeliac disease

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Hashimoto's
thyroiditis - Some
type 2. Mostly
type 4.
Granuloma
annulare

Autoimmune
disease, receptor Graves' disease IgM or IgG
V
mediated (see
Myasthenia gravis Complement
below)

Type V
This is an additional type that is sometimes (especially in the UK) used as a distinction from Type 2.[7]

Instead of binding to cell surfaces, the antibodies recognise and bind to the cell surface receptors, which either prevents
the intended ligand binding with the receptor or mimics the effects of the ligand, thus impairing cell signaling.

Some clinical examples are:

Graves' disease
Myasthenia gravis

The use of Type 5 is rare. These conditions are more frequently classified as Type 2, though sometimes they are specifically
segregated into their own subcategory of Type 2.

See also
Type I hypersensitivity
Type II hypersensitivity
Type III hypersensitivity
Type IV hypersensitivity
Type V hypersensitivity
Intolerance

References
1. Gell PGH, Coombs RRA, eds. Clinical Aspects of Immunology. 1st ed. Oxford, England: Blackwell; 1963. Section IV,
Chapter 1
2. Black, C. A. (1999). "Delayed type hypersensitivity: Current theories with an historic perspective" (http://escholarship.
org/uc/item/2fw0g1xx). Dermatology Online Journal. 5 (1): 7. PMID 10673450 (https://www.ncbi.nlm.nih.gov/pubmed/
10673450).
3. Delayed Hypersensitivity Reactions (https://emedicine.medscape.com/article/136118-overview) at eMedicine
4. Kumar, Vinay; Abbas, Abul K.; Aster, Jon C., eds. (2014). "Hypersensitivity: Immunologicaly Mediated Tissue Injury"
(https://books.google.com/books?id=5NbsAwAAQBAJ&pg=PA200). Robbins & Cotran Pathologic Basis of Disease
(9th ed.). Elsevier Health Sciences. pp. 200–11. ISBN 978-0-323-29635-9.
5. Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson (2007). "Table 5-1". Robbins Basic
Pathology (8th ed.). Philadelphia: Saunders. ISBN 1-4160-2973-7.
6. Le, Tau. First Aid for the USMLE Step 1 2013, p. 203-204

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