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Type I
hypersensitivity is an inappropriate immune response to harmless foreign
antigen to which the individual is previously sensitized. This allergic
reaction is usually IgE-mediated, which induces mast cells and basophils activation
1. It occurs within minutes of exposure to the antigen (also termed
immediate hypersensitivity), may be local as well as systemic. Severity ranges
from irritating (hay fever) to fatal (systemic anaphylaxis).

An
allergic reaction occurs in 2 sequences:

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1)     
primary
exposure of sensitization

2)     
subsequent
exposure

Primary exposure of sensitization

An allergen
is inhaled and acquired by an antigen-presenting cell (APC), such as dendritic
cell or B cells. Dendritic cell migrates to the lymph nodes and present it to a
CD4 T cell. Naïve T cell gets activated and differentiates into TH2 cell 2.

In the
other hand, B cell was bound to an allergen. It processes the antigen and
displays class II MHC-peptide complexes on the surface. B cell binds to the TH2
cell through TCR-MHC interaction and by CD40-CD40L interaction 2, 3.

The TH2
cell releases cytokines such as IL-4, IL-5 and IL-13 upon subsequent exposure with
the antigen. IL-4 stimulates the differentiation of TH2 cells and class
switching of B cell to IgE-producing plasma cell. IL-5 develops and activates
eosinophils, which release toxic substances that can damage host cells. IL-13
enhances IgE production and stimulates epithelial cells to secrete mucus.

Secreted IgE binds
to the high affinity receptor (Fc?RI) of mast cells and basophils. This end the
sensitization phase.

 

 

 

 

 

 

Figure 1 showed the key steps in T- and B-cell collaboration to
produce antibodies during sensitization.

 

 

 

 

Subsequent exposure

A subsequent
re-exposure to the same allergen triggers the cross linking of IgE antibodies,
which result in mast cells degranulation and release of pro-inflammatory
mediators that give the clinical effect seen in an allergic reaction 4,5.

Type I hypersensitivity
reactions can be classified into early and late phase reactions.

Early phase reactions occur within
minutes of the second exposure and may subside within 60 minutes. Some of the
preformed mediators contained in the mast cells granules are histamine, enzymes
like chymase, tryptase and eosinophilic chemotactic factors.

o  
Histamine
causes smooth muscle contraction of the airways making it more difficult to
breath. It also causes vasodilation and increased vascular permeability. Thus,
local blood flow increased and leakage of fluid through vessels causing edema
and swelling 4, 5.

o  
Enzymes
cause tissue damage and lead to generation of kinins and complements leading to
further inflammation 4.

o  
Eosinophilic
chemotactic factors recruits eosinophils to the affected site and are
implicated in later phase reactions.

Late phase reactions occur 2-24
hours later without additional allergen exposure. They may last for several
days and are due to infiltration of eosinophils, neutrophils, monocytes, CD4 T
cells as well as sustained epithelial tissue inflammation. Newly synthesized
mediators include arachidonic acid derivatives (leukotrienes, prostaglandins)
and cytokines will be released.

o  
Leukotriene
C4 and D4 are several thousand times more potent than histamine in causing
smooth muscle constriction and vascular permeability. Leukotriene B4 is a
neutrophil chemotaxis 4, 5.

o  
Prostaglandin
D2 produced mainly in mast cells cause bronchoconstrictive and vasodilating
effect. It also increased mucus secretion 5.

o  
Cytokines
include IL-1 and TNF-? are pro-inflammatory cytokines that promotes leukocytes
influx 4, 5.

 

 

 

 

 

 

 

 

 

References

1)     
Stephen J Galli, M. T. (2012). IgE and mast cells in allergic
disease. Nature Medicine, 693-704.

2)     
Alberts B, J. A. (2002). Molecular Biology of the Cell.
4th edition. T Cells and MHC Proteins. New York: Garland Sciences.

3)     
Agrawal, R. G. (2013). Clinical View on the Importance of
Dendritic Cells in Asthma. Expert Review of Clinical Immunology,
899-919.

4)     
Janeway CA Jr, T. P. (2001). Immunobiology: The Immune
System in Health and Disease. 5th edition. Effector mechanisms in allergic
reactions. New York: Garland Science.

5)     
Oettgen, O. T. (2011). Beyond immediate hypersensitivity:
evolving roles for IgE antibodies in immune homeostasis and allergic diseases. Immunological
Reviews, 128-143.

 

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