Immunity
was originally considered a protective process helping the body to overcome
infectious agents and their toxins. However, immune response may sometimes
be harmful to the host. Sensitized individual respond to subsequent antigenic
stimuli in an inappropriate or exaggerated manner leading to tissue damage, disease
or even death. The term 'hypersensitivity' thus refers to the injurious
consequences in the sensitized host following contact with specific antigen.
The initial contact with antigens called sensitizing dose sensitizes
appropriate B or T cells and the subsequent dose of same antigen called
shocking dose produces abnormal reactions.
Exposure to antigen activates B cells to form IgE secreting plasma cells.
Author: Judith A Owen; Jenni Punt; Sharon A
Stranford; Patricia P
Jones; Janis Kuby
Publisher: New York: W.H. Freeman, ©2013.
Therefore,
hypersensitivity is an abnormal immune response which produces damage either
histopathological or physiological in the host.
Types
of Hypersensitivity
Hypersensitivity
as classified by Gell and Coomb are of 4 types:
•Type
I: Anphylatic or IgE mediated hypersensitivity
•Type
II: Antibody mediated cytoxicity
•Type
III: Immune complex mediated hypersensitivity
•Type
IV: Cell mediated hypersensitivity
Types
of Hypersensitivity
•Immediate:
Type I, II and III are immediate type of hypersensitivity since the symptoms
are manifest within minutes or hours after a sensitized recipient encounters
antigen.
•Delayed: Type IV is delayed type of hypersensitivity because
of the delay of symptoms until days after exposure.
Type
I Hypersensitivity
Also called as IgE mediated or Reagin
mediated or anaphylatic immediate type of hypersensitivity.
Antigens that induce Type I hypersensitivity include pollen, fungal
spores, insect venom, animal danders, mites, helminthic infections, etc.
Mechanism
of Type I hypersensitivity
Exposure to antigen activates B cells to form IgE secreting plasma cells.
The secreted IgE molecules
bind to IgE specific Fc receptors on the mast cells and
blood basophiles.
Thus, Fab fragments of IgE remains
exposed.
Upon re-exposure to the
same antigen, antigen gets attached to the free Fab fragments
of IgE bound on mast cells.
This results in the cross linking
of IgE molecules.
The
cross linking triggers the biochemical signals which stimulates the
phospholipid metabolism that opens channels in the cell membrane, thus leading
to calcium influx.
As a result, an energy dependent disorganisation of intracellular granules
occurs with the eventual release of granules contents in the extracellular
fluid.
The granule contents are the vasoactive amines such as histamins,
heparin, Eosinohpile chemotactic factors for anaphylaxis (ECFA), Neutrophil
chemotactic factor (NCFA), etc.
These causes smooth muscle contraction,
increased vascular permeability and vasodilation.
The phospholipid metabolism
makes the arachidonic acid available which generates prostaglandins and
leukotrienes.
Prostaglandins cause vascular dilation and leukotrienes cause
smooth muscle contractions.
The mast cells also secrete cytokines such as TNF,
IL-4 and IL-5 which promotes the recruitment of eosinophiles to the site of
their release and cause inflammation.
Eosinophiles and neutrophiles
release protease which causes the neighbouring tissue damage.
Typical manisfestation
include systemic anaphylaxis and localized anaphylaxis such as hay fever,
asthama, hives, food allergies, eczema, etc.
References
1. Kuby
immunology
Publisher: New York: W.H. Freeman, ©2013.
Edition:
7th edition
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