Allergy pathophysiology

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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

  1. 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.
  2. 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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