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{{Allergy}}
{{Allergy}}
{{CMG}}
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==Overview==
==Overview==
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==Pathophysiology==
==Pathophysiology==
The [[pathophysiology]] of allergic responses can be divided into two phases. The first is an [[Acute (medical)|acute response]] that occurs immediately after exposure to an allergen. This phase can either subside or progress into a "late phase reaction" which can substantially prolong the symptoms of a response, and result in tissue damage.
There are two stages to the pathophysiology of allergic reactions. The first is an allergic reaction that occurs shortly after being exposed to an allergen. This phase can either fade away or progress into a "late phase reaction," which can significantly prolong the symptoms of an allergic reaction and cause tissue damage.<ref name="pmid18650915">{{cite journal |vauthors=Galli SJ, Tsai M, Piliponsky AM |title=The development of allergic inflammation |journal=Nature |volume=454 |issue=7203 |pages=445–54 |date=July 2008 |pmid=18650915 |pmc=3573758 |doi=10.1038/nature07204 |url=}}</ref>


===Acute Response===
===Acute Response===
[[Image:Allergy degranulation processes 01.svg|thumb|left|Degranulation process in allergy.'''1''' - antigen; '''2''' - IgE antibody; '''3''' - FcεRI receptor; '''4''' - preformed mediators (histamine, proteases, chemokines, heparine); '''5''' - [[granules]]; '''6''' - [[mast cell]]; '''7''' - newly formed mediators (prostaglandins, leukotrienes, thromboxanes, PAF)]]
In the early stages of acute response:
In the early stages of allergy, a type I hypersensitivity reaction against an allergen, encountered for the first time, causes a response in a type of immune cell called a [[T helper cell|T<sub>H</sub>2 lymphocyte]], which belongs to 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.


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]]s into the surrounding tissue causing several systemic effects, such as [[vasodilation]], [[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 particular body systems; asthma is localized to the respiratory system and eczema is localized to the [[dermis]].
{{Family tree/start}}
{{Family tree | | | | A01 | | | |A01= Early stage of [[Allergy]] or [[Type 1 hypersensitivity]] reaction}}
{{Family tree | | | | |:| | | | | }}
{{Family tree | | | | B01 | | | |B01= Encounter of [[allergen]] with [[T-helper cell]]}}
{{Family tree | | | | |:| | | | | }}
{{Family tree | | | | C01 | | | |C01= [[IL-4]] production}}
{{Family tree | | | | |:| | | | | }}
{{Family tree | | | | D01 | | | |D01= [[T<sub>H</sub>2 cells]] stimulated by [[IL-4]] started interacting with [[B-cell]]}}
{{Family tree | | | | |:| | | | | }}
{{Family tree | | | | E01 | | | |E01= Production of [[antibody]] [[IgE]], and binding with [[IgE-specific receptor]] (a kind of [[Fc receptor]] called [[FcεRI]] on [[mast cells]] and [[basophils]]}}
{{Family tree | | | | |:| | | | | }}
{{Family tree | | | | F01 | | | |F01= Acute inflammatory response and Sensitization of IgE coated cell to allaergen}}
{{Family tree/end}}
 
In the late stage of acute response:
{{Family tree/start}}
{{Family tree | | | | A01 | | | |A01= Binding of similar [[allergen]] to [[IgE coated]] [[mast cells]] and [[basophils]] }}
{{Family tree | | | | |:| | | | | }}
{{Family tree | | | | B01 | | | |B01= Cross-linking of the [[IgE]] and [[Fc receptors]]}}
{{Family tree | | | | |:| | | | | }}
{{Family tree | | | | C01 | | | |C01= Activation and Degranulation of [[mast cells]] and [[basophils]]}}
{{Family tree | | | | |:| | | | | }}
{{Family tree | | | | D01 | | | |D01= Release of [[histamine]] and other inflammatory chemical mediators ([[cytokine]]s, [[interleukin]]s, [[leukotriene]]s, and [[prostaglandin]]s)}}
{{Family tree | | | | |:| | | | | }}
{{Family tree | | | | E01 | | | |E01= Production of [[antibody]] [[IgE]], and binding with [[IgE-specific receptor]] (a kind of [[Fc receptor]] called [[FcεRI]] on [[mast cells]] and [[basophils]]}}
{{Family tree | | | | |:| | | | | }}
{{Family tree | | | | F01 | | | |F01= Systemic effects: [[vasodilation]], [[mucous]] secretion, [[nerve]] stimulation and [[smooth muscle]] contraction}}
{{Family tree/end}}
 
Acute inflammatory response causes systemic inflammatory reaction like [[vasodilation]], [[mucous]] secretion, [[nerve]] stimulation and [[smooth muscle]] contraction. Rhinorrhea, itchiness, dyspnea, and anaphylaxis are all symptoms of this. The symptoms may 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) depending on the individual, allergen, and mode of introduction.


===Late-phase Response===
===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>{{cite journal |author=Grimbaldeston MA, Metz M, Yu M, Tsai M, Galli SJ |title=Effector and potential immunoregulatory roles of mast cells in IgE-associated acquired immune responses |journal=Curr. Opin. Immunol. |volume=18 |issue=6 |pages=751–60 |year=2006 |pmid=17011762 |doi=10.1016/j.coi.2006.09.011}}</ref> Cytokines from mast cells may also 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>{{cite journal |author=Holt PG, Sly PD |title=Th2 cytokines in the asthma late-phase response |journal=Lancet |volume=370 |issue=9596 |pages=1396–8 |year=2007 |pmid=17950849 |doi=10.1016/S0140-6736(07)61587-6}}</ref>
Late phase responses are common after the chemical mediators of the acute response have subsided. This is due to the migration of other leukocytes to the initial site, such as neutrophils, lymphocytes, eosinophils, and macrophages. The reaction appears 2–24 hours after the initial reaction.<ref>{{cite journal |author=Grimbaldeston MA, Metz M, Yu M, Tsai M, Galli SJ |title=Effector and potential immunoregulatory roles of mast cells in IgE-associated acquired immune responses |journal=Curr. Opin. Immunol. |volume=18 |issue=6 |pages=751–60 |year=2006 |pmid=17011762 |doi=10.1016/j.coi.2006.09.011}}</ref> Mast cell cytokines may also contribute to the persistence of long-term effects. Although late phase responses in asthma are slightly different from those seen in other allergic reactions, they are still triggered by eosinophil mediator release and are still dependent on TH2 cell activity.<ref>{{cite journal |author=Holt PG, Sly PD |title=Th2 cytokines in the asthma late-phase response |journal=Lancet |volume=370 |issue=9596 |pages=1396–8 |year=2007 |pmid=17950849 |doi=10.1016/S0140-6736(07)61587-6}}</ref>


==References==
==References==

Latest revision as of 06:48, 23 March 2021

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Marufa Marium, M.B.B.S[2]

Overview

There are two stages to the development of an allergic reaction: acute and late-phase reaction. The body's reaction depends a lot on the phase and how far chemical mediation has progressed.

Pathophysiology

There are two stages to the pathophysiology of allergic reactions. The first is an allergic reaction that occurs shortly after being exposed to an allergen. This phase can either fade away or progress into a "late phase reaction," which can significantly prolong the symptoms of an allergic reaction and cause tissue damage.[1]

Acute Response

In the early stages of acute response:

 
 
 
Early stage of Allergy or Type 1 hypersensitivity reaction
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Encounter of allergen with T-helper cell
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
IL-4 production
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
[[TH2 cells]] stimulated by IL-4 started interacting with B-cell
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Production of antibody IgE, and binding with IgE-specific receptor (a kind of Fc receptor called FcεRI on mast cells and basophils
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Acute inflammatory response and Sensitization of IgE coated cell to allaergen
 
 
 

In the late stage of acute response:

 
 
 
Binding of similar allergen to IgE coated mast cells and basophils
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Cross-linking of the IgE and Fc receptors
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Activation and Degranulation of mast cells and basophils
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Release of histamine and other inflammatory chemical mediators (cytokines, interleukins, leukotrienes, and prostaglandins)
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Production of antibody IgE, and binding with IgE-specific receptor (a kind of Fc receptor called FcεRI on mast cells and basophils
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Systemic effects: vasodilation, mucous secretion, nerve stimulation and smooth muscle contraction
 
 
 

Acute inflammatory response causes systemic inflammatory reaction like vasodilation, mucous secretion, nerve stimulation and smooth muscle contraction. Rhinorrhea, itchiness, dyspnea, and anaphylaxis are all symptoms of this. The symptoms may 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) depending on the individual, allergen, and mode of introduction.

Late-phase Response

Late phase responses are common after the chemical mediators of the acute response have subsided. This is due to the migration of other leukocytes to the initial site, such as neutrophils, lymphocytes, eosinophils, and macrophages. The reaction appears 2–24 hours after the initial reaction.[2] Mast cell cytokines may also contribute to the persistence of long-term effects. Although late phase responses in asthma are slightly different from those seen in other allergic reactions, they are still triggered by eosinophil mediator release and are still dependent on TH2 cell activity.[3]

References

  1. ↑ Galli SJ, Tsai M, Piliponsky AM (July 2008). "The development of allergic inflammation". Nature. 454 (7203): 445–54. doi:10.1038/nature07204. PMC 3573758. PMID 18650915.
  2. ↑ Grimbaldeston MA, Metz M, Yu M, Tsai M, Galli SJ (2006). "Effector and potential immunoregulatory roles of mast cells in IgE-associated acquired immune responses". Curr. Opin. Immunol. 18 (6): 751–60. doi:10.1016/j.coi.2006.09.011. PMID 17011762.
  3. ↑ Holt PG, Sly PD (2007). "Th2 cytokines in the asthma late-phase response". Lancet. 370 (9596): 1396–8. doi:10.1016/S0140-6736(07)61587-6. PMID 17950849.

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