Editing Hypersensitivity (section)

==Gell and Coombs classification==
The Gell and Coombs classification of hypersensitivity is the most widely used, and distinguishes four types of immune response that result in bystander tissue damage.<ref>{{Cite journal|date=July 2008|title=Davidson's Principles and Practice of Medicine, IE Edition, 20th Ed: Medicine—Clinical Medicine|journal=Journal of Endocrinology, Metabolism and Diabetes of South Africa|language=en|volume=13|issue=2|pages=75|doi=10.1080/22201009.2008.10872174|issn=1608-9677|s2cid=220276722|doi-access=free}}</ref>
{| class="wikitable sortable"
|+Immunologic aspects of hypersensitivity reactions
!     Type     !! style="width: 150px" | Alternative names     !! style="width: 120px" | Antibodies or Cell Mediators      !!     Immunologic Reaction    !!     Examples
|-

! [[Type I hypersensitivity|I]]
|
* [[Allergy]]
* Immediate
* [[Anaphylaxis|Anaphylactic]]
||
* [[Immunoglobulin E|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 [[vasoactivity|vasoactive]] biomolecules. Testing can be done via skin test for specific IgE.<ref name=":1" />||
* [[Atopy]]
* [[Anaphylaxis]]
* [[Asthma]]
* [[Eosinophilic granulomatosis with polyangiitis]]
|-
! [[Type II hypersensitivity|II]]
|
* [[antibody-dependent cell-mediated cytotoxicity|Antibody-dependent]]
||
* [[Immunoglobulin M|Antibody IgM]]
* [[Immunoglobulin G|Antibody IgG]]
* [[Complement system|Complement]]
* [[Membrane attack complex]] (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 [[Membrane attack complex|MAC]]. Testing includes both the direct and indirect [[Coombs test]].<ref name=":2" />||
* [[Autoimmune hemolytic anemia]]
* [[Rheumatic heart disease]]
* [[Thrombocytopenia]]
* [[Erythroblastosis fetalis]]
* [[Goodpasture's syndrome]]
* [[Graves' disease]]
* [[Myasthenia gravis]]
* [[Pemphigus vulgaris]]
|-
! [[Type III hypersensitivity|III]]
|
* [[Immune complex]]
||
* [[Immunoglobulin G|Antibody IgG]]
* [[Complement system|Complement]]
* [[Neutrophil]]s
| 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.<ref name="Robbins">{{cite book |chapter=Hypersensitivity: Immunologicaly Mediated Tissue Injury |chapter-url=https://books.google.com/books?id=5NbsAwAAQBAJ&pg=PA200 |pages=200–11 |editor1-first=Vinay |editor1-last=Kumar |editor2-first=Abul K. |editor2-last=Abbas |editor3-first=Jon C. |editor3-last=Aster |year=2014 |title=Robbins & Cotran Pathologic Basis of Disease |edition=9th |publisher=Elsevier Health Sciences |isbn=978-0-323-29635-9}}</ref>||
* [[Serum sickness]]
* [[Rheumatoid arthritis]]
* [[Arthus reaction]]
* [[Post streptococcal glomerulonephritis]]
* [[Membranous nephropathy]]
* [[Reactive arthritis]]
* [[Lupus nephritis]]
* [[Systemic lupus erythematosus]]
* [[Hypersensitivity pneumonitis|Extrinsic allergic alveolitis]] ([[hypersensitivity pneumonitis]])
|-
! [[Type IV hypersensitivity|IV]]

|
* Delayed,<ref name=":1">{{cite journal |pmid=10673450 |url=http://escholarship.org/uc/item/2fw0g1xx |year=1999 |last1=Black |first1=C. A. |title=Delayed type hypersensitivity: Current theories with an historic perspective |journal=Dermatology Online Journal |volume=5 |issue=1 |pages=7 |doi=10.5070/D32FW0G1XX |url-access=subscription }}</ref><ref name=":2">{{EMedicine|article|136118|Delayed Hypersensitivity Reactions}}</ref>
* [[Cell-mediated immunity|cell-mediated immune memory response]],
* Antibody-independent
* Cytotoxic
||Cells
* [[T-cells]]
**[[Cytotoxic T cell]]s (CTLs)
**[[T helper cell]]s
| CTLs and T helper cells (specifically T<sub>h</sub>1 and T<sub>h</sub>17 cells)<ref>{{Cite book|last=Abbas|first=Abul K.|title=Cellular and Molecular Immunology|date=6 May 2021 |publisher=Elsevier|isbn=978-0-323-75748-5|pages=444}}</ref> 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.<ref name="LeTau">Le, Tau. First Aid for the USMLE Step 1 2013, p. 203-204</ref>||
* [[Contact dermatitis]], including [[Urushiol-induced contact dermatitis]] (poison ivy rash).
* [[Mantoux test]]
* [[Chronic transplant rejection]]
* [[Multiple sclerosis]]<ref name="Kumar5-1">{{cite book |chapter=Table 5-1 |author1=Mitchell, Richard Sheppard |author2=Kumar, Vinay |author3=Abbas, Abul K. |author4=Fausto, Nelson |title=Robbins Basic Pathology|publisher=Saunders |location=Philadelphia |year= 2007 |isbn=978-1-4160-2973-1 |edition=8th}}</ref>
* [[Coeliac disease]]
* [[Hashimoto's thyroiditis]]
* [[Granuloma annulare]]
|}