Allergy pathophysiology: Difference between revisions
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Revision as of 06:41, 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
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
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.