Hypersensitivity refers to
undesirable reactions produced by the
normal immune system,
including allergies and autoimmunity
These reactions may be damaging,
uncomfortable, or occasionally fatal.
Type I – Immediate, Atopic,
Type II – Antibody Dependent
Type III – Immune Complex
Type IV – Cell Mediated / Delayed
Type Of Hypersensitivity
TYPE I. Immediate OR Anaphylactic
Type I hypersensitivity is also known as
or anaphylactic hypersensitivity.
The reaction may involve skin (urticaria
and eczema), eyes (conjunctivitis),
nasopharynx (rhinorrhea, rhinitis),
bronchopulmonary tissues (asthma) and
gastrointestinal tract (gastroenteritis).
Mediated by IgE antibody to specific
The primary cellular component in this
hypersensitivity is the mast cell or
The reaction is amplified and/or
modified by platelets, neutrophils and
Mast cells stimulated and release
Most of the IgE in the body is bound
with high affinity receptors (Fc
epsilonRI), found on mast cells and
The cells are activated by cross-linking
of Fc epsilonRI receptors via antigen
binding to the bound IgE molecules.
Such cross-linking leads to rapid
degranulation of the mast cells and the
release of primary inflammatory
mediators stored in the granules.
Mast cell activation via Fc epsilonRI also
leads to the production of two other
types of mediators. These secondary
Molecules SOME SPACES Effects
Theophylline OR epinephrine -prolongs or
increases cAMP levels in mast cells which
Cromolyn Sodium Prevents release of
Type II Hypersensitivity
The second class of damaging reactions
is caused by specific antibody binding to
cells or tissue antigens.
The antibodies are of the IgM or IgG
classes and cause cell destruction.
It involves binding of antibodies (IgG or
IgM) to cell surface antigen or
extracellular matrix molecules.
Antibody directed to cell surface
antigens can activate complement to
damage the cells.
Red Blood cell
with Ag on cell
IgG binds to Ag
compliment lysis red
cell (cell death)
The result may be complement
mediated lysis as occurs in
ABO Transfusion Reactions.
Pencillin allergy also belong to this
Type III (Immune-Complex Mediated)
Due to the formation of antigen-antibody
complexes, also called immune-
Type III hypersensitivity is mediated by
immune complexes essentially of IgG
When antibody combines with specific
antigen, immune complexes are formed.
Normally they are promptly removed by
Occasionally, they persist and deposit in
tissues resulting in disorders.
In persistent microbial or viral infections,
immune complexes may be deposited in
organs eg. Kidneys - resulting in
dysfunction, in joints – arthirits, in BV –
Wherever the immune complexes are
deposited, they cause inflammation and
Type IV Hypersensitivity
This is the only class of hypersensitive
reactions to be triggered by antigen -
specific T lymphocyte cells (not
Cell mediated hypersensivity is induced
mainly in skin.
When skin again comes in contact with
those agents, the sensitized person
develops erythema, itching, eczema or
necrosis within 12 – 48 hours.
The Langerhans cell in the epidermis
interacts with CD4 T cells to cause
It occurs after sensitisation with simple
chemicals, (e.g nickel & formaldehyde),
plant materials (Ivy poison, Oak poison),
topically applied drugs (sulfonamides &
neomycin), some cosmetics and soaps.
(a) In the sensitization phase after initial
contact with antigen (e.g., peptides
derived from intracellular bacteria), TH
cells proliferate and differentiate into
TH1 cells. Cytokines secreted by these
T cells are indicated by the dark blue
(b) In the effector phase after subsequent
exposure of sensitized TH1 cells to
antigen, the TH1 cells secrete a variety
of cytokines and chemokines. These
factors attract and activate macrophages
and other nonspecific inflammatory cells.
Activated macrophages are more
effective in presenting antigen, thus
perpetuating the DTH response, and
function as the primary effector cells in
A prolonged DTH response can lead to
formation of a granuloma, a nodule-
like mass. Lytic enzymes released
from activated macrophages in a
granuloma can cause extensive tissue
Allergic contact dermatitis
Corticosteroids and other immunosuppressive
agents are used in treatment.
Comparison of Different Types of hypersensitivity
antibody IgE IgG, IgM IgG, IgM None
antigen exogenous cell surface soluble tissues & organs
15-30 minutes minutes-hours 3-8 hours 48-72 hours
antibody antibody antibody T-cells
SLE, farmer's lung
Allergic Contact Dermatitis
ACD accounts for approximately 20% of all
ACD is a type IV, delayed or
cell-mediated immune reaction
that is elicited when the skin
comes in contact with a chemical
to which an individual has been
Synonyms include contact dermatitis and
ACD is a type IV hypersensitivity
Requires prior sensitization to the
Once sensitized a low concentration of
causative chemical elicits a response
Clinical Features of ACD
Patchy and diffuse distributions may be
seen with body washes and shampoos
Treatment of ACD
Involves identification of causative
Clear the dermatitis with topical, or if
necessary systemic corticosteroids
Complete and prolonged clearing can
take up to 6 weeks or more, even when
allergens are being avoided
Most common allergen
tested by the NACDG,
with 14% of patients
Reacting to it.
Commonly used in jewelry,
Buckles and other metal
nickel allergy should
avoid custom jewelry
and can usually wear
stainless steel or gold.
Most commonly used
topical antibiotic used
with other antibacterial
Agent e.g Bacitracina &
Polymixin, as well as
Co-reactivity is commonly seen with
neomycin and bacitracin
Thimerosal is used as a preservative.
Most sensitization may be due to its use
as a preservative in vaccines.
Other exposures include:
o Contact lens solution
o Otic and opthalmic solutions
o Antiseptics and
Systemic Contact Dermatitis
Systemic exposure to a chemical may
result in a diffuse dermatitis
Patient has had a prior contact allergy
and then becomes exposed through a
systemic route, such as injection, oral,
intravenous, or intranasal administration
One of most
is patient with
Asthma is a condition characterized by
reversible bronchospasm and chronic
inflammation of airway passages.
Individuals with asthma appear to
produce large amounts of the Antibody
IgE that attach to the mast cells present
in many tissues.
Exposure to a trigger such as pollen
will result in the allergen-binding mast
cell-bound IgE, which in turn causes the
release of inflammatory mediators such
as Histamine and Leukotrienes.
The response of a patient with asthma
to these triggers can be divided into
an ―early phase‖ and a ―late phase.‖
Early Phase of Asthma
The early phase of asthma is characterized by:
a. Marked constriction of bronchial airways
b. Difficulty in breathing
c. Production of excess mucus.
The bronchospasm that occurs may be the
result of the increased release of certain
inflammatory mediators such as histamine,
prostaglandins and bradykinin that, in the early
stages of asthmatic response, promote
bronchoconstriction rather than inflammation.
Late Phase of Asthma
The late phase of asthma can occur several hours
after the initial onset of symptoms and manifests
mainly as an inflammatory response.
The primary mediators of inflammation during the
asthmatic response are the white blood cells
Eosinophils that stimulate mast cell degranulation
and release substances that attract other white cells
to the area.
Subsequent infiltration of the airway tissues with
white blood cells such as Neutrophils and
lymphocytes also contributes to the overall
inflammatory response of the late phase of asthma.
Some Potential Asthma Triggers..
Allergens — Pollen, pet dander, fungi,
Respiratory tract infections
Sign and Symptoms
Shortness of breath
Chest tightness and pain
Staging of Severity
Type Day Attacks Night Attacks
Mild Intermittant < 2 times in a week < twice in a month
Mild Persistant > 2 times in a week > Twice in a month
> 3 times in a week
> 4 times in a
Severe Persistant Continous or At
Type Quicker Relief Long Term
Mild Intermittant Short Acting B2
Short Acting B2
Mild Persistant Short Acting B2
Low Dose Inhaled
SR Theophylline OR
Short Acting B2
High Dose Inhaled
Low Dose Inhaled
Steroid + Short
Acting B2 Agonist
Short Acting B2
Inhaled Steroid +