Allergy pathophysiology: Difference between revisions

	Allergy Microchapters
Home
Patient Information
Overview
Historical Perspective
Pathophysiology
Causes
Differentiating Allergies from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Allergy pathophysiology On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Allergy pathophysiology All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Allergy pathophysiology
CDC on Allergy pathophysiology
Allergy pathophysiology in the news
Blogs on Allergy pathophysiology
Directions to Hospitals Treating Allergies
Risk calculators and risk factors for Allergy pathophysiology

VisualWikitext

Latest revision as of 06:48, 23 March 2021

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

[[T_H2 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

↑ 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.
↑ 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.
↑ 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.

Template:WikiDoc Sources

[pmid18650915-1] 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.

[1]

[2]

[3]

@@ Line 1: / Line 1: @@
 {{Allergy}}
-{{CMG}}
+{{CMG}} {{AE}} {{MMT}}
 __NOTOC__
 ==Overview==
-The development of allergic response occurs in two phases: acute and late-phase reaction. The body's response varies largely on the type of phase and the advancement of chemical mediation.
+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==
-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===
-[[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===
-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==
 {{reflist|2}}
+{{WikiDoc Help Menu}}
+{{WikiDoc Sources}}
 [[Category:Dermatology]]
@@ Line 30: / Line 60: @@
 [[Category:Ophthalmology]]
 [[Category:Immune system]]
-[[Category:Primary care]]
-{{WikiDoc Help Menu}}
-{{WikiDoc Sources}}