it is especially related to veterinary sciences

2. HYPERSENSITIVITY
ALSO CALLED ALLERGY OR ANAPHYLAXIS

3. 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

4. 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
Definitions

5. 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)

6. 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

7. 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

8. Continue…
 B-cell + antigen plasma cell IgE Binds to Fc-receptor on
mast cell Release of vasoactive amines Action of mediators on
effector organs

9. 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

10. 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

11. Antigen on the
surface of the
cell
antibodies
Complement C1
Antibody and
complement
bind to the cell
Cell lysis
Ag Ag
Ab
C1
Formation
of MAC
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

12. 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.

13. 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

14. 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)

15. 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

16. 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

17. 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