Hypersensitivity

Hypersensitivity
Specialty	Immunology

Hypersensitivity (also called hypersensitivity reaction or intolerance) refers to undesirable reactions produced by the normal immune system, including allergies and autoimmunity. They are usually referred to as an over-reaction of the immune system and these reactions may be damaging, uncomfortable, or occasionally fatal. Hypersensitivity reactions require a pre-sensitized (immune) state of the host. The Gell and Coombs classification of hypersensitivity is the most widely used, and distinguishes four types of immune response which result in bystander tissue damage.[1]

Gell and Coombs classification

Immunologic aspects of hypersensitivity reactions
Type	Alternative names	Antibodies or Cell Mediators	Immunologic Reaction	Often mentioned disorders
I	Allergy Immediate Anaphylactic	Antibody IgE	Fast response which occurs in minutes, rather than multiple hours or days. Free antigens cross link the IgE on mast cells and basophils which causes a release of vasoactive biomolecules. Testing can be done via skin test for specific IgE.[2]	Atopy Anaphylaxis Asthma Churg-Strauss Syndrome
II	Cytotoxic, Antibody-dependent	Antibody IgM Antibody IgG Complement MAC	Antibody (IgM or IgG) binds to antigen on a target cell, which is actually a host cell that is perceived by the immune system as foreign, leading to cellular destruction via the MAC. Testing includes both the direct and indirect Coombs test.[3]	Autoimmune hemolytic anemia Rheumatic heart disease Thrombocytopenia Erythroblastosis fetalis Goodpasture's syndrome Graves' disease[note 1] Myasthenia gravis[note 1]
III	Immune complex	Antibody IgG Complement Neutrophils	Antibody (IgG) binds to soluble antigen, forming a circulating immune complex. This is often deposited in the vessel walls of the joints and kidney, initiating a local inflammatory reaction.[4]	Serum sickness Rheumatoid arthritis Arthus reaction Post streptococcal glomerulonephritis Membranous nephropathy Reactive arthritis Lupus nephritis Systemic lupus erythematosus Extrinsic allergic alveolitis (hypersensitivity pneumonitis)
IV	Delayed,[2][3] cell-mediated immune memory response, Antibody-independent	Cells T-cells	T helper cells (specifically T_h1 cells) are activated by an antigen presenting cell. When the antigen is presented again in the future, the memory Th1 cells will activate macrophages and cause an inflammatory response. This ultimately can lead to tissue damage.[5]	Contact dermatitis, including Urushiol-induced contact dermatitis (poison ivy rash). Mantoux test Chronic transplant rejection Multiple sclerosis[6] Coeliac disease Hashimoto's thyroiditis Granuloma annulare
V	Autoimmune	IgM or IgG Complement	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.	Graves' disease Myasthenia gravis

Notes

See type V explanation in table.

References

"Davidson's Principles and Practice of Medicine, IE Edition, 20th Ed: Medicine—Clinical Medicine". Journal of Endocrinology, Metabolism and Diabetes of South Africa. 13 (2): 75. July 2008. doi:10.1080/22201009.2008.10872174. ISSN 1608-9677. S2CID 220276722.
Black, C. A. (1999). "Delayed type hypersensitivity: Current theories with an historic perspective". Dermatology Online Journal. 5 (1): 7. PMID 10673450.
Delayed Hypersensitivity Reactions at eMedicine
Kumar, Vinay; Abbas, Abul K.; Aster, Jon C., eds. (2014). "Hypersensitivity: Immunologicaly Mediated Tissue Injury". Robbins & Cotran Pathologic Basis of Disease (9th ed.). Elsevier Health Sciences. pp. 200–11. ISBN 978-0-323-29635-9.
Le, Tau. First Aid for the USMLE Step 1 2013, p. 203-204
Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson (2007). "Table 5-1". Robbins Basic Pathology (8th ed.). Philadelphia: Saunders. ISBN 978-1-4160-2973-1.
Rajan, T.V. (2003). "The Gell–Coombs classification of hypersensitivity reactions: A re-interpretation". Trends in Immunology. 24 (7): 376–9. doi:10.1016/S1471-4906(03)00142-X. PMID 12860528.

External links

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[:0-4] See type V explanation in table.

[1] "Davidson's Principles and Practice of Medicine, IE Edition, 20th Ed: Medicine—Clinical Medicine". Journal of Endocrinology, Metabolism and Diabetes of South Africa. 13 (2): 75. July 2008. doi:10.1080/22201009.2008.10872174. ISSN 1608-9677. S2CID 220276722.

[:1-2] Black, C. A. (1999). "Delayed type hypersensitivity: Current theories with an historic perspective". Dermatology Online Journal. 5 (1): 7. PMID 10673450.

[:2-3] Delayed Hypersensitivity Reactions at eMedicine

[Robbins-5] Kumar, Vinay; Abbas, Abul K.; Aster, Jon C., eds. (2014). "Hypersensitivity: Immunologicaly Mediated Tissue Injury". Robbins & Cotran Pathologic Basis of Disease (9th ed.). Elsevier Health Sciences. pp. 200–11. ISBN 978-0-323-29635-9.

[LeTau-6] Le, Tau. First Aid for the USMLE Step 1 2013, p. 203-204

[Kumar5-1-7] Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson (2007). "Table 5-1". Robbins Basic Pathology (8th ed.). Philadelphia: Saunders. ISBN 978-1-4160-2973-1.

[pmid12860528-8] Rajan, T.V. (2003). "The Gell–Coombs classification of hypersensitivity reactions: A re-interpretation". Trends in Immunology. 24 (7): 376–9. doi:10.1016/S1471-4906(03)00142-X. PMID 12860528.