Editing Allergy (section)

==Pathophysiology==
[[File:The Allergy Pathway.jpg|thumb|A summary diagram that explains how allergy develops]]
[[File:Tissues Affected In Allergic Inflammation.jpg|thumb|Tissues affected in [[allergic inflammation]]]]

===Acute response===
[[File:Allergy degranulation processes 01.svg|thumb|Degranulation process in allergy. Second exposure to allergen. '''1''' – antigen; '''2''' – IgE antibody; '''3''' – FcεRI receptor; '''4''' – preformed mediators (histamine, proteases, chemokines, heparin); '''5''' – [[granule (cell biology)|granules]]; '''6''' – [[mast cell]]; '''7''' – newly formed mediators (prostaglandins, leukotrienes, thromboxanes, [[Platelet-activating factor|PAF]]).]]
In the initial stages of allergy, a type I hypersensitivity reaction against an allergen encountered for the first time and presented by a professional [[antigen-presenting cell]] causes a response in a type of immune cell called a [[T helper cell|T<sub>H</sub>2 lymphocyte]], a subset of [[T cell]]s that produce a [[cytokine]] called [[interleukin-4]] (IL-4). These T<sub>H</sub>2 cells interact with other [[lymphocytes]] called [[B cell]]s, whose role is production of antibodies. Coupled with signals provided by IL-4, this interaction stimulates the B cell to begin production of a large amount of a particular type of antibody known as IgE. Secreted IgE circulates in the blood and binds to an IgE-specific receptor (a kind of [[Fc receptor]] called [[FcεRI]]) on the surface of other kinds of immune cells called [[mast cell]]s and [[basophil]]s, which are both involved in the acute inflammatory response. The IgE-coated cells, at this stage, are sensitized to the allergen.<ref name=Janeway/>

If later exposure to the same allergen occurs, the allergen can bind to the IgE molecules held on the surface of the mast cells or basophils. Cross-linking of the IgE and Fc receptors occurs when more than one IgE-receptor complex interacts with the same allergenic molecule and activates the sensitized cell. Activated mast cells and basophils undergo a process called [[degranulation]], during which they release [[histamine]] and other inflammatory chemical mediators ([[cytokine]]s, [[interleukin]]s, [[leukotriene]]s, and [[prostaglandin]]s) from their [[granule (cell biology)|granules]] into the surrounding tissue causing several systemic effects, such as [[vasodilation]], [[mucus|mucous]] secretion, [[nerve]] stimulation, and [[smooth muscle]] contraction.

This results in [[rhinorrhea]], itchiness, dyspnea, and anaphylaxis. Depending on the individual, allergen, and mode of introduction, the symptoms can be system-wide (classical anaphylaxis) or localized to specific body systems. Asthma is localized to the respiratory system and eczema is localized to the [[dermis]].<ref name="Janeway" />

===Late-phase response===
After the chemical mediators of the acute response subside, late-phase responses can often occur. This is due to the migration of other [[leukocyte]]s such as [[neutrophil]]s, [[lymphocyte]]s, [[eosinophil]]s, and [[macrophage]]s to the initial site. The reaction is usually seen 2–24 hours after the original reaction.<ref name="Effector and potential immunoregulatory roles of mast cells in IgE-associated acquired immune responses"/> Cytokines from mast cells may play a role in the persistence of long-term effects. Late-phase responses seen in asthma are slightly different from those seen in other allergic responses, although they are still caused by release of mediators from eosinophils and are still dependent on activity of T<sub>H</sub>2 cells.<ref name="Th2 cytokines in the asthma late-phase response"/>

===Allergic contact dermatitis===
Although [[allergic contact dermatitis]] is termed an "allergic" reaction (which usually refers to type I hypersensitivity), its pathophysiology involves a reaction that more correctly corresponds to a [[type IV hypersensitivity]] reaction.<ref>{{cite journal | vauthors = Martín A, Gallino N, Gagliardi J, Ortiz S, Lascano AR, Diller A, Daraio MC, Kahn A, Mariani AL, Serra HM | title = Early inflammatory markers in elicitation of allergic contact dermatitis | journal = BMC Dermatology | volume = 2 | pages = 9 | date = August 2002 | pmid = 12167174 | pmc = 122084 | doi = 10.1186/1471-5945-2-9 | doi-access = free }}</ref> In type IV hypersensitivity, there is activation of certain types of [[T cells]] (CD8+) that destroy target cells on contact, as well as activated [[macrophage]]s that produce [[hydrolytic enzyme|hydrolytic]] [[enzyme]]s.<ref name="c364">{{cite book | last1=Hou | first1=Wanzhu | last2=Xu | first2=Guangpi | last3=Wang | first3=Hanjie | title=Treating Autoimmune Disease with Chinese Medicine | chapter=Basic immunology and immune system disorders | publisher=Elsevier | year=2011 | isbn=978-0-443-06974-1 | doi=10.1016/b978-0-443-06974-1.00001-4 | pages=1–12}}</ref>