• Normally the immune response remove Ag by

various mechanisms without extensive

damage to host tissue.
• Under certain circumstances, this
inflammatory response can have a harmful
effects resulting in significant tissue damage.
• This inappropriate immune response is
termed Hypersensitivity
• Hypersensitivity :This word implies an
increased immune response
• but instead its an inappropriate
immune response to an Ag
• Hypersensitivity occurs in the course of
either humoral or cellular immunity

• Two scientists : Gell and Coombs Proposed

a classification in which hypersensitivity
reaction are divided into 4 types
 Classification of hypersensitivity (hs)

• Type I IgE mediated hs

• Type II Ab mediated cytotoxic hs

• Type III immune complex

mediated hs
type IV delayed type hs
 Type I hs (IgE mediated hs)
• Ag that induced type I hs called Allergen. like
• Pollen
• House dust mite
• Penicillin
• Egg
• Animal dander
• Wasp venom
 1. Allergen cross the Ag binding site of Ab on
the surface of B –cells
2. Activation of Th2 cell and IL-4 and IL-5
secretion
First exposure to allergen 3. Activation of B-cell and differentiation into
plasma cell and memory cells
4. Plasma cell will secret IgE Ab
5. IgE will bind IgE specific Fc receptor on
mast cell and Basophils . These cells called
sensitized cells.
Second exposure to the same allergen
1. Allergen will cross linking the
bound IgE on the surface of
mast cell and basophile
(sensitized cell)
2. This leads to degranulation
of mast cell and basophile and
release of pharmacologically
active mediators
from the granules
3- these mediators act on
surrounding tissues causing
vasodilatation, smooth muscle
contraction and increased
vascular permeability
 Types of mediators
1. Primary mediators: produced before degranulation
and stored in the granules (histamine, serotonin
and eosinophil chemotactic factor)
2. Secondary mediators: are synthesized after
target-cell activation or by break-down membrane
phospholipids (platelet activating factor,
prostaglandin, bradykinin and leukotrienes.
 End results of this hs
1. Immediate hypersensitivity reaction: occurs within
minutes after repeated exposure to allergen.
2. Late-phase reaction: 2-4 hours after repeated
exposure to allergen. This is due to the migration
of other leukocytes such as
neutrophils, lymphocytes, eosinophils,
and macrophages to the initial site.

- Cytokines from mast cells may also play a role in the

persistence of long-term effects. Late phase
responses seen in asthma
 Clinical manifestations
1. Systemic anaphylaxis: it is a shock-like state and
often fatal and occurs within minutes. (penicillin, bee venome).
Shock: A serious condition that occurs when the cardio-vascular
system is unable to supply enough blood flow to the body,
causing inadequate tissue perfusion.

2- Localized anaphylaxis: this reaction is limited to

a specific target tissue or organ (allergic rhinitis,
asthma). This is usually occur in atopic persons.
• Atopy : Increased in the IgE level in genetically
susceptible individual who is predispose to have
allergy against common environment Ag.
• Diagnosis:
In vitro:
1-Radio Immuno Sorbent Test (RIST):
This test measure the total amount of IgE in the
serum.
• Radio Allergo Sorbent Test 2-
• (RAST)This test measure the total amount of IgE
specific for a particular allergen in the serum
• In vivo:
• - Skin prick test
 Treatment
1. Avoidance of allergen
2. Drugs: antihistamines,epinephrine,theophylline,
sodium chromoglycate,cortisone
3- Immunotherapy:
a- by repeated injections of increasing doses of
allergens leads to Tolerance induction, this is called
hyposensitization .
causes a shift towards IgG (IgG4) production by a
shift to Th1 subsets and INF-γ and IL-10 production
and turn off IgE response . This is called blocking Ab.
b- Monoclonal Abs against IgE Fc region
 Anaphylactoid reaction
• The clinical manifestation of anaphylaxis can occur in
the absence of any evidence of an allergen-IgE Ab
events.
• These reaction arise through the non immunological
release of vasoactive amines and inflammatory
mediators in certain susceptible individuals.
-(i.v. radiographic contrast media, succinylcholine,
and morphine and idiopathic)