Allergy pathophysiology
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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
- ↑ 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.