Hypersensitivity immunology M.Sc ppt.pdf

Hypersensitivity is an inappropriate or exaggerated immune response to an antigen that can cause tissue damage.

2. GOVT. JAJWLYADEV NAVEEN GIRLS COLLEGE JANJGIR (C.G)
SESSION –2025-26

3. TOPIC - HYPERSENSITIVITY
•GUIDED BY –
• Dr. Ajay Mahant Sir
•Guest Lecturer
•Department of zoology
•SUBMITTED BY –
•Gudiya yadaw
•Class – M. Sc 3rd Semester
•Subject – Paper 3rd(Zoology)

4. CONTENT
1) Introduction(what is hypersensitivitiy)
2) Type of hypersensitivity reaction
a)Type 1 – Ab mediated hypersensitivity
b)Type 2- Cytotoxic mediated
c)Type 3 – Immune complex mediated
d)Type 4 – Delay(T-cell mediated )
3) Hypersensitivity pathway
•Type 1 – hypersensitivity
a)Local anaphylaxis(Two phase)
b)Systemic Anaphylaxis
•Type 2 – hypersensitivity
a)Mechanism 1 – Complement Dependent reaction
b)Mechanism 2 – Ab Mediated Cellular Cytotoxicity
c)Mechanism 3 – AB Mediated cellular Dyfunction
•Type 3 – hypersensitivity
•Type 4 – hypersensitivity
a)Delayed Type hypersensitivity
b)Cell mediated cytotoxicity
4) Conclusion
5)Reference

5. 1) Introduction
•Exaggerated or misdirected immune
response
•Result in tissue injury or other
pathophysiological changes
•Occure when an alrady sensitized
individual is re-exposed to the same
foreign substance
•May be immediate or delyed
•Ensuring tissue injury may be caused
by:
•1 Release of vasoactive substances
•2 phagocytosis or lysis of cells
•3 Activation of inflammatory &
cytolytic components of
complements system
•4 Release of cytokines , proteolytic
enzymes and other mediators of
tissue injury or inflammation

6. 2) Types of Hypersensitivity
1) Type 1 – Ab Mediated
•IgE (With 1 hours)
•Anaphylaxis
•Histamine Secrated by -mast
cell
2) Type 2 – Cytotoxic mediated
•IgG or IgM
•Response time (hour to day
•Attack on host cell –
endogenus
•Heamylytic Anamia – Auto
immune disease
3) Type 3 – Immune Complex
Mediators
•Response timing – 1-3 weak
•Complement system
involvement
•Serum sickness – lepus disease
4) Type 4 – Delay (T Cell mediated)
•Response timing – day to weak
•Ex.Rasis – Skin disease

7. 3) Hypersensitivity Pathway
1)Type 1 hypersensitivity
mechanism
•Immediate/Anaphylactic type
•IgE – mediated
•Occur Within minutes
•Provided by re-exposure to the
same Ag(by contact , inhalation ,
ingestion or injection)
•It has two types of response :
Local or systemic
•Local anaphylaxis has two phase
•Initial response
•Late phase

8. a) Local Anaphylaxis
•Atopy – genetically determined
predisposition to develop
localized anaphylactic reaction to
inhaled or ingested allergens
•(+) family history – chromosome
5q31
•With higher serum IgE level
compared to general population
•Local anaphylaxis has two phase:
a) Initial response –
vasodilation,vascular leakage,
smooth muscle spasm or
glandular secretion – 5-30 min
after exposer – subside in 60
minutes
b) Late phase reaction – 2-8 hours
later without additional exposure
to antigen – more intence
infiltration of tissues with
eosinophils, neutrophils,
basophils , monocytes & CD4+
Tcell – with mucosal epithelial
damage

9. b) Systemic Anaphylaxis
•Occur ofter administration of heterologous protein
(e.g.antisera),hormones , enzyme ,polysaccharide &
dregs
•Exposer – itching , hives & skin erythema –
contraction of respiration bronchioles + respiration
distress (+) laryngeal edema

10. 2) Type 2- hypersensitivity
a) Mechanism 1:Complement
Dependent Reactions
•Antibody-complement-
mediated lysis
•Antibody(IgM / IgG) + ag on
cell surface-mac

11. b) Mechanism 2 :Ab mediated cellular cytotoxicity
•Due to NK activity – non-
sensitized cells with Fc
recepters
•Ab-Ag – activation of NK
cell- bind to Fc fragment of
IgG –cell lysis without
phagocytosis
•Destruction of targets too
large to be phagocytosed
(parasites ,tumer cell)+ graft
rejection

12. c) Mechanism 3: Ab mediated cellular Dyfunction
•Ach Receptorted blocked by
Ab
• Ach not bind with their
receptors
•Disturbe heart muscles
contraction
•Ab direct against this cell
surface receptor
•Inpair or diregulation
function
•Ex. Grave disease
•Erthroblastocytis fetalis

13. Over all process summary (Type ll

14. 3) Type lll hypersensitivity

15. Type lll hypersensitivity mechanism

16. 4) Type 4 hypersensitivity

17. Type 4 hypersensitivity:2forms
a) delayed-type hypersensitivity
•Mediated dy cd4 t cells
•1
st
exposure to ag – CD4 T cell +
class ll MHC– differentiation of
naive CD4 T cells to TH1 Cells –
Release OF IL- 12 IFN Gama,IL-2 &
lymphotoxin
•Tuberculin skin test, contact
dermatitis, granulomatous
inflammation

18. b) cell –mediated cytoxicity
•-mediated by CD 8+ t-
cells
•Sensitized CD 8+ t-cell
kill antige-bearing
target cells
•Graft rejection,virus
infections,tumor
immunity
•Two mechanisms:
•1 perforin-granzyme-
dependent Killing-cause
perforation of plasma
membrane
•2 Fas-FasL dependent ki
lling –activation of
apoptosis

19. 4) Conclusion
•Hypersensitivity conlude with the body’s immune system
causing an abnormal and damaging reaction to a substance
•This overreaction can range from mild allergies to life –
threatening condition like Anaphylaxis
•The main way to control it is avoid the triggering substance ,
but medication can also help