hypersensitivity Undesirable reactions produced by the normal immune system. Hypersensitivity is an exaggerated immune response that results in tissue damage and is manifested in the individual on a second or subsequent contact with an antigen. Hypersensitivity reactions can be classified as either immediate or delayed. Obviously immediate reactions appear faster than delayed ones, but the main difference between them is the nature of the immune response to the antigen.

1. Hypersensitivities

2. NISAR ALI
MSC Mi crobi ol ogy
emai l
Ni sar4044@yahoo. com
University of Swat

3. Undesirable reactions produced by the normal
immune system. Hypersensitivity is an exaggerated
immune response that results in tissue damage and is
manifested in the individual on a second orsubsequent
contact with an antigen.
Hypersensitivity reactions can be classified as either
immediate ordelayed. Obviously immediate reactions
appearfasterthan delayed ones, but the main difference
between themis the nature of the immune response to
the antigen.
Allergy
Allergies, also known as allergic diseases, are a number
of conditions caused by hypersensitivity of the
immune system to something in the environment that
usually causes little orno problemin most people. These
diseases include hay fever, food allergies,
atopic dermatitis, allergic asthma, and anaphylaxis
. Symptoms may include red eyes, an itchy rash,
runny nose, shortness of breath, orswelling.

4. General Features
1.Hypersensitivity reactions can be elicited by exogenous
environmental antigens orendogenous self antigens.
2.Results fromfailure of normal regulation of immune
response.
3.Development of hypersensitivity diseases is often
associated with the inheritance of particularsusceptibility
genes.

5. Types Of Hypersensitivity
Hypersensitivity reactions are divided according to
mechanismof action into fourgroups:
1-Type I (Immediate hypersensitivity).
2-Type II (Cytotoxic hypersensitivity).
3-Type III (Immune complex hypersensitivity).
4-Type IV (Cell-mediated orDelayed hypersensitivity).
5-Type V (Stimulatory Type) Jones-Mote Reaction (or)
Cutaneous Basophil Hypersensitivity

6. Type IHypersensitivity (IGEDEPENDENT)
A type I hypersensitive reaction is induced by certain
types of antigens referred to as allergens, and has all the
hallmarks of a normal humoral response. Allergic reactions
occurwhen an individual who has produced IgE antibody
in response to an innocuous antigen (allergen)
subsequently encounters the same allergen. Type I, or
anaphylactic, reactions often occurwithin 2 to 30 minutes
aftera person sensitized to an antigen is re-exposed to
that antigen.

7. PHASES OFTYPEIHypersensitivity REACTION
IMMEDIATE REACTION LATE-PHASE REACTION
Manifested in minutes Manifested in 2-24 hours later
Subsides in few hours May last forseveral days
Release of mast cell
•Histamine
•Leukotrienes: C4, D4
•Prostaglandins: D2
Tissue infiltration by:
•Neutrophils
•Eosinophils
•Basophils
•Monocytes
•CD4+ T Cells
Effects
•Vasodilation
•Increase Vascular Permeability
•Bronchoconstriction
•Mucus-secretion
•Epithelial injury by inflammatory
response

8. Type IIHypersensitivity
(Cytolysis And Cytotoxic).
These reactions involve a combination of IgG (orIgM)
antibodies with an antigenic determinants on the surface
of cells. Antibody can activate the complement system,
creating pores in the membrane of a foreign cell, orit can
mediate cell destruction by antibody dependent cell-
mediated cytotoxicity (ADCC). Type II hypersensitivity is
generally, called cytolytic orcytotoxic reactions because it
results in the destruction of host cells, either
by lysis ortoxic mediators. Type II hypersensitive
reactions involve antibody-mediated destruction of cells

9. Type II hypersensitivity

10. Type IIIHypersensitivity—Immune Complex-
Mediated
Type III reactions involve antibodies against soluble
antigens circulating in the serum. The antigen-antibody
complexes are deposited in organs and cause inflammatory
damage. The tissue damage that results fromthe
deposition of immune complexes is caused by the
activation of complement, platelets and phagocytes; in
essence, an acute inflammatory response

11. Immune complex-mediated hypersensitivity. (1) Immune complexes on the basement
membrane of the wall of a blood vessel, where they; (2) activate complement and
attract inflammatory cells such as neutrophils to the site. (3) The neutrophilis discharge
enzymes as they react with the immune complexes, resulting in damage to tissue cells

12. Type IV Hypersensitivity—Delayed Hypersensitivity
Type IV hypersensitivity reactions (delayed
hypersensitivity) constitute one aspect of cell-mediated
immune response and are caused mainly by T cells. These
are typically provoked by intracellularmicrobial infections
orhaptens like simple chemicals applied on the skin,
evolve slowly and consist of a mixed cellularreaction
involving lymphocytes and macrophages in particular. It is
named delayed hypersensitivity because it appears in 24 to
48 hours afterthe presensitized host encounters the
antigen, while immediate hypersensitivity reactions
develop in 1/2 to 12 hours. A majorfactorin the delay is
the time required forthe participating T cells and
macrophages to migrate to and accumulate nearthe
foreign antigens. The T cells involved in delayed type
hypersensitivity reactions are primarily TDcells. In some
types of hypersensitivities resulting in tissue damage, Tc
cells may also participate.

13. Type IV (delayed orcell-mediated) hypersensitivity

15. Type V: Hypersensitivity (Stimulatory Type)
Jones-Mote Reaction (or) Cutaneous Basophil
Hypersensitivity
This is an antibody-mediated hypersensitivity and is a
modification of type II hypersensitivity reaction.
Antibodies interact with antigens on cell surface which
leads to cell proliferation and differentiation instead of
inhibition orkilling. Antigen-antibody reaction enhances
the activity of affected cell.
Example of Grave’s disease: Thyroid hormones are
produced in excess quantity in grave’s disease. Long acting
thyroid stimulating (LATS) antibody is an autoantibody to
thyroid membrane antigen. It is presumed that LATS
combines with a TSHreceptoron thyroid cell surface and
brings about the the same effect as TSHresulting in
excessive secretion of thyroid hormone.