Allergy pathophysiology: Difference between revisions
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===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)]] | [[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)]] | ||
{{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}} | |||
{{Family tree/end}} | |||
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]]. | 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]]. |
Revision as of 06:21, 23 March 2021
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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.
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 | |||||||||||||||||||
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 (cytokines, interleukins, leukotrienes, and prostaglandins) from their granules 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.
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 leukocytes such as neutrophils, lymphocytes, eosinophils and macrophages to the initial site. The reaction is usually seen 2-24 hours after the original reaction.[1] 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 TH2 cells.[2]
References
- ↑ 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.