HYPERSENSITIVITY

ALSO CALLED ALLERGY OR ANAPHYLAXIS

Antigen and Antibody Response

There are two important features of immune response

1) Immunity
2) Hypersensitivity

 When an antigen gets entry to the body, antibodies are produced which is
termed as PROPHYLAXIS
 In contrast to that, it may also leads to HYPERSENSITIVITY or ALLERGY

 Common features of immunity and hypersitivity:

i. Both are specific in action
ii. Both involve body cells
iii. Both are induced by protein substances
iv. Both results in union between antigen and antibody
Definitions

1) Altered type of immune response to some substances

2) An exaggerated immune response that result in tissue damage and is manifested in the
individual on second or subsequent contact with the antigen
Classification of Hypersensitivity

 Generally Hypersensitivity is classified as:

1) Immediate type (reactions are faster)
2) Delayed (reactions are delayed)

 Peter Gell and Robert Coombs (1963) developed a system of classification for
hypersensitivity.
 Gell-Coombs classification consist of 4 hypersensitivity reactions:
1. Type I hypersensitivity (Anaphylaxis)
2. Type II hypersensitivity (Cytotoxic)
3. Type III hypersensitivity (Immune Complex)
4. Type IV hypersensitivity (Cell-mediate)
 Type I hypersensitivity

 It is immediate type
 Allergic type of reactions recurring immediately following an individual’s
second contact with responsible antigen (allergen), which further react with
antibody associated with tissue cells and leading to release of
pharmacologically active substances
 The major class of antibody responsible for it is IgE class of antibody instead
of IgA, IgD or IgM
Sequence of Events In Type I

 Antigen contact leads to production of sensitizing antibodies by

B-lymphocyte. The antibody is usually IgE class of antibody
 IgE binds to specific elements Fc-receptor on surface of cellular elements i.e. mast cell
 Release of vasoactive amine substance (mainly Histamine, serotonin)
 These vasoactive amine stimulates smooth muscle contraction, vascular leakage, late
phase inflammation and intestinal hyper-motility
 Symptoms of anaphylactic shock is observed
Continue…

 B-cell + antigen plasma cell IgE Binds to Fc-receptor on mast

cell Release of vasoactive amines Action of mediators on effector organs
Type II Hypersensitivity

 It is generally called antibody mediated cytolytic or cytotoxic reaction

 It results in destruction of host cell
 Antibody involve is IgG and IgM
 These antibody causes tissue destruction by recruiting and activating inflammatory cells
and the complement system
 The antibody act as a bridge between antigen and effectors
 Mechanism of Type II

1. Complement activation
(complement mediated lysis of cell)
2. Recruitment and activation of leukocytes
(Neutrophils and macrophage)
 The antibody dependent cytoxicity is an important
in causing pathological damage or cell destruction.
Following are the condition involved:
i. Transfusion reaction
ii. Hemolytic disease of newborn
iii. Homograft rejection
iv. Autoimmune hemolytic anemia
 Ag Ag
Formation
of MAC
antibodies

Ab
Antigen on the
surface of the
cell
C1
Complement C1

Antibody and
complement Cell lysis
bind to the cell

Activation of complement and formation of cytocidal membrane attack complex(MAC)

after binding of IgM and some class of IgG to their specific antigen, which causes osmotic
lysis of cell
Type III Hypersensitivity

 First observation was made by Maurice Arthus (1903)

 Also called Immune complex hypersensitivity
 Immune complexes are the formation of antigen-antibody complexes in serum, with
subsequent deposition of the complexes in the tissue is the most important feature of type
III hypersensitivity
Drug-antibody complexes precipitate on vascular walls, complement is
activated, and an inflammatory reaction is triggered.
 Mechanism of Type III

 Three steps involved

i. Immune complex formation
ii. Increased vascular permeability
Immune complex activates complement system.
Complement C3a, C4a, C5a split products are anaphylotoxin
that cause localized mast cell activation and its degranulation.
Further these causes basophil and platelets to release mediators
such as Histamine and other. These increase in vascular permeability.
iii. Vasculitis
The increased vascular permeability allows immune complex to
be deposit in vascular wall
Type of Type III

 There are two types of type III hypersensitivity

1. Localized (immune complex deposits locally with in tissue)
2. Generalized (large quantities are deposited in circulation)
Type IV Hypersensitivity

 Tissue damage mediated by T-lymphocyte, also called Cell-mediated hypersensitivity

 Delayed hypersensitivity because manifestations seen after 2-3 days of exposure to
sensitizing antigen.
 E.g. in contact demitits, photosensitization
Mechanism

1) Antigen binds to tissue cell activate CD4+ T-lymphocyte and CD8+

Lymphocyte secrete cytokines activate macrophage Delayed
type hypersensitivity
2) CD8+ cytotoxic lymphocyte
directly lyse target cell
bearing MHC I associated
foreign antigen, without
precipitation of
macrophage or any other
effector mechanism
Reference

 Veterinary immunology, Basic concept and application

By Y Hari Babu

Special Thanks to:

Dr. Shakoor Ahmad
Presented By:
Ihtisham Ul Haq
(student of DVM at aup.edu.pk)
Ihtishamulhaq114@gmail.com