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77 hypersensitivity.pptx
1. HYPERSENSITIVITY
• NAME- Kiran Khatua
• REGD NO- 200705180077
• SUBJECT- Immunology and cancer biology
• BATCH- M .Sc zoology 2nd semester
• SESSION- 2020-2022
• GUIDED BY- Dr. Sitaram Swain
DEPARTMENT OF ZOOLOGY
SCHOOL OF APPLIED SCIENCE, BHUBANESWAR
3. Introduction
• Hypersensitivity is the inappropriate
response of immune system to certain
antigens present in the environment,
leading to tissue damage or even death.
• It refers to undesirable reactions produced
by normal immune system including
allergies and autoimmunity.
• Both the humoral and cell mediated arms
of the immune response may participate in
hypersensitivity reactions.
4.
5. Type I Hypersensitivity
• Type I hypersensitivity reaction is
commonly called allergic or immediate
hypersensitivity reaction.
• Type I reaction are also known ad IgE
mediated hypersensitivity reaction
• IgE is responsible for sensitizing mast cells
and providing recognition of antigen for
immediate hypersensitivity reactions.
• The reaction can occur in two forms :
anaphylaxis and atopy.
• Later we discuss its mechanism from
figure.
7. Type II Hypersensitivity
• Type II hypersensitivity is also known as cytotoxic
hypersensitivity and may affect a variety of organs
and tissues.
• The antibodies which are involved in cell destruction
in this hypersensitivity are IgG and IgM .
MECHANISM OF TYPE II
• Two different antibody mediated mechanisms are
these hypersensitivity reaction;
1. Complement mediated
2. Antibody dependent cell mediated cytotoxicity.
8.
9. Type III Hypersensitivity
• It is a immediate hypersensitivity reaction mediated by
the formation of immune complexes.
• The type III hypersensitivity reactions occur when the
body exposed to an antigen , which is not cell bound.
MECHANISM:
• Type III hypersensitivity reaction develops when
immune complex activates C3a and C5a
components of complement system.
• C3a and C5a are lymph toxin (anaphylotoxin) that
causes localized mast cell degranulation.
• Degranulation of mast cell releases histamine
which increases vascular permeability of blood
capillaries. This facilitates deposition of immune
complexes on wall of blood vessel.
• C5a, C3a and C5b67 also acts as chemotatic
factors for neutrophils, So it attracts neutrophils at
the site of immune complex deposition.
10. Cont.
• C3b acts as opsonin by binding with immune
complex. Neutrophil binds to C3b coated immune
complex by means of type I complement receptor
which is specific for C3b.
• The neutrophils attempt to phagocytose the
immune complex but phagocytosis is not possible
because immune complexes are deposited on
basement membrane, so the neutrophil releases
lytic enzymes to destroy immune complex.
• The lytic enzymes cause tissue damage surrounding
of immune complex deposits, resulting
hypersensitivity reaction. Furthermore complement
proteins can also contribute to tissue destruction.
11.
12. Type IV Hypersensitivity
• It is a cytokine mediated inflammatory
response resulting from the sensitization of
T Lymphocytes.
• It is also called as delayed type
hypersensitivity.
MECHANISM :
• Caused by inflammation resulting from
cytokines produced by CD4+ TCells and cell
killing by CD8+ Tcells.
• Lets see and discuss it from figure.
13.
14. Reference
• Basu , S . and Banik ,K.B. (2018). Hypersensitivity :
An overview . Immunology: current Research ;2
(1),1-2 .
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