Hypersensitivity refers to excessive or inappropriate immune responses that are harmful to the body. There are four main types of hypersensitivity reactions based on their pathogenic mechanisms: 1. Type I reactions are immediate or anaphylactic and mediated by IgE antibodies, causing release of inflammatory mediators from mast cells. 2. Type II reactions are antibody-dependent cytotoxic reactions, where antibodies bind to antigens on self cells leading to complement activation and cell lysis. 3. Type III reactions are immune complex-mediated, where circulating antigen-antibody complexes deposit in tissues and activate complement, causing inflammation. 4. Type IV reactions are cell-mediated and involve activation of sensitized T cells by antigens,

1. IMMUNOLOGY
DONE BY:
NIVETHA.M
1st M.Sc ZOOLOGY

2. INTRODUCTION:
• Hypersensitivity refers to excessive, undesirable
reactions produced by the normal immune system.
• This reaction leads to damage, discomfort and
sometimes fatal to the body.
• It is an appropriate response of repeated exposure to
antigen.
• The immune response becomes injurious to the host.
• Hypersensitivity reactions develop in the course of
either a humoral or a cell mediated immune response.

3. Factors causing hypersensitivity
• Factors causing hypersensitivity – allergens
• In clinical terms ,hypersensitivity is called allergy
• Extrinsic factors & intrinsic factors
Drugs – Penicillin, Aspirin, Sulphamide
Airborne particles – Pollen grains, spores, animal
dander's
Food stuffs – Shell fish, vegetables, peanut
Blood transfusion of mismatched blood
Infectious organisms – bacteria, viruses, fungi, parasite

4. Hypersensitivity Reactions
 Hypersensitivity reactions divided into two types
 Local reactions – When the symptoms appear in a
restricted area.
 Systemic reactions – When the symptoms affect all
the organ systems of the body.

5. TYPES OF HYPERSENSITIVITY
HYPERSENSITIVITY
BASED ON
TIME TAKEN
FOR THE
REACTION
IMMEDIATE
HYPERSENSITIVITY
DELAYED
HYPERSENSITIVITY
BASED ON
DIFFERENT
MECHANISMS OF
PATHOGENS
TYPE 1 TYPE 2 TYPE 3 TYPE 4 TYPE 5

6. BASED ON TIME TAKEN FOR THE REACTION
1) IMMEDIATE HYPERSENSITIVITY
• When the immune reactions manifest in a short duration
of time ,within minutes.
• E.g.: Most of hypersensitivities to drugs (penicillin)
• Inflammatory responses occurs in a few minutes.
• This immune reaction appears and disappears rapidly.
• It involves the interaction of antigen and antibody.
• It is handled by B-cells by the production of antibodies
.
• It is inhibited by antihistamine drugs.

7. Cont…
2) DELAYED HYPERSENSITIVITY
• When the immune reactions manifest slowly from 24
hours to 72 hours.
• It appears slowly & lasts longer.
• It produces erythema, indurations and lymphocyte
infiltration.
• They involves the reaction between antigens & T
cells.
• Cell mediated immunity.
• They are suppressed by corticosteroids.

8. BASED ON THE DIFFERENT MECHANISMS
OF PATHOGENESIS
• Coombs & Gell proposed 5 types of hypersensitivity.
• Type 1 – Anaphylactic hypersensitivity
• Type 2 – Antibody dependent cytotoxic
hypersensitivity
• Type 3 – Immune complex mediated
hypersensitivity
• Type 4 – Cell mediated hypersensitivity
• Type 5 – Stimulatory hypersensitivity

9. Type 1 – Immediate or Atopic or Anaphylactic
Hypersensitivity
• Type I hypersensitivity is an allergic reaction provoked by re-exposure to a specific
antigen.
• Exposure may be by due to ingestion, inhalation, injections or direct contact.
• The reaction is mediated by IgE antibodies and produced by the immediate release of
histamine, tryptase, arachidonate and derivatives by basophils and mast cells.
• This causes an inflammatory response leading to an immediate (within seconds to
minutes) reaction.
• The reaction may be either local or systemic.
• Symptoms vary from mild irritation to sudden death from anaphylactic shock.
• Treatment usually involves epinephrine, antihistamines and corticosteroids

10. MECHANISM OF TYPE 1 HYPERSENSITIVITY
• When a person receives the allergens
it get attached to the B cells.
• The allergens stimulate the B cells to
change into plasma cells.
• The plasma cells make IgE antibodies.
• These antibodies are called reagins.
• The IgE antibodies produced for the
first time, get attached to the surface
receptors of mast cell with the help of
their Fc segment.

11. Allergen cross reacting with IgE on
mast cell

12. The next time the allergen enters the body, it cross-links the Fab portions of the IgE
bound to the mast cell. This triggers the mast cell to degranulate, that is, release its
histamine and other inflammatory mediators. The inflammatory mediators are now
able to bind to receptors on target cells which leads to dilation of blood vessels,
constriction of bronchioles, excessive mucus secretion, and other symptoms of
allergy.

13. Cont..
• As this initial contact with antigens leads to the priming
of the B cells , it is known as sensitizing or priming
dose.
• Subsequent contact with the allergen causes
manifestation of hypersensitivity – shock dose.
• When the animal get exposed to the second antigen for
the second time ,the IgE antibodies attached to the
surface of mast cells ,bind the antigen.
• The allergens cross link the IgE antibodies attached to
the mast cells.
• This triggers the mast cells where a series of enzymatic
reaction occurs.

14. • This results in the mast cells to release the granules –
degranulation.
• These granules contain substances like histamine,
serotonin ,heparin etc ..
• These substances are the primary cause for
anaphylactic hypersensitivity.
• The manifestation of anaphylaxis are due to mediators.
• These are of 2 types
Primary mediators
Secondary mediators
• The primary mediators include :- histamine, serotonin,
heparin.

15. • Secondary mediators are produced by leucocytes upon the
stimulation of mast cells.
• These include :- slow reacting substance of anaphylaxis
(SRS-A) ,prostaglandins ,platelet activating factor.
• Some examples are
Allergic asthma
Allergic conjunctivitis
Allergic rhinitis ("hay fever")
Anaphylaxis
Angioedema
Urticaria (hives)

16. Type II - antibody-dependent cytotoxic
hypersensitivity
• In type II hypersensitivity, the antibodies produced
by the immune response bind to antigens on the
patient's own cell surfaces.
• The antigens recognized in this way may either be
intrinsic ("self" antigen, innately part of the
patient's cells) or extrinsic (absorbed onto the cells
during exposure to some foreign antigen, possibly
as part of infection with a pathogen).

17. Cont..
• IgG and IgM antibodies bind to these antigens to
form complexes that activate the classical pathway
of complement activation for eliminating cells
presenting foreign antigens (which are usually, but
not in this case, pathogens).
• As a result mediators of acute inflammation are
generated at the site and membrane attack
complexes cause cell lysis and death.
• The reaction takes hours to a day.

18. • These reactions are classified into 2 types,
ISOIMMUNE REACTION
AUTOIMMUNE REACTION
ISOIMMUNE REACTION
Reaction brought about by the antigen and
antibody of two individuals belonging to the same
species.
1. Transfusion reaction
2. Erythroblastosis foetalis
3. transplant rejection reaction

19. Cont..
AUTO IMMUNE REATION
• Reaction brought about by the interaction of antigen
and antibody of the same individual.
• It include autoimmune hemolytic anaemia.
• The individuals produces antibodies against his own
RBC antigens.
• The red cell coated with antibodies are destroyed in
the spleen and liver.

20. MECHANISMS OF CYTOTOXIC REACTION
 In this reaction the cell damage occurs in following steps,
1) PHAGOCYTOSIS
 The antibodies are attached to the cell surface antigen
 Then the macrophage bind to the antibody coated cells
 The macrophages engulf the antibody coated cells
2) LYSIS
 The antibody coated cells bind to the phagocytic cells through their
receptor for C3b
 They move continue to fix in sequence up to the lytic c8 and c9
components to cause damage to the cells by the mechanisms similar to
that in lysis
3) KILLING
 The antibody coated cells may be attacked by cytotoxic killer cells
which carry receptor for C3b and Fc portion of IgG

22. EXAMPLES
• Autoimmune haemolytic anaemia
• Pernicious anemia
• Immune thrombocytopenia
• Transfusion reactions
• Hashimoto's thyroiditis
• Graves' disease
• Myasthenia gravis
• Farmer's Lung
• Hemolytic disease of the newborn

23. TYPE 3 HYPERSENSITIVITY
• It is mediated by immune complexes essentially of
IgG and IgM antibodies with suitable antigens.
• Antibody – antigens complexes form in proper
concentration of antigen and antibody.
• Depending on the size of these complexes they
may be cleared efficiently by phagocytic cells.

24. MECHANISMS OF TYPE 3 HYPERSENSITIVITY
• When enormous amount of soluble antigens enter the body ,
antibodies are produced by B cells.
• This result in antigen – antibody complex.
• The immune complexes then get attached to in and around
minute capillaries.
• And they bind to complement.
• The compliment 3(C3) and 5(C3) produce active factors
called anaphylotoxin and chemotoxin.
• Anphylotoxin triggers the mast cells to release vasoactive
amines.
• The amines increases the tissue permeability.
• Chemotoxin attracts the polymorphs and promote
phagocytosis resulting in the release oh hydrolytic enzymes.

27. Examples:
• Immune complex glomerulonephritis
• Rheumatoid arthritis
• Serum sickness
• Subacute bacterial endocarditis
• Symptoms of malaria
• Systemic lupus erythematosus
• Arthus reaction

28. TYPE 4 HYPERSENSITIVITY
• It is caused by the interaction between antigens
and sensitized T cells.
• Lead to inflammatory reaction result in tissue
damage.
• Antibodies are not involved here.
• As T cells are involved – cell mediated
hypersensitivity.
• Also delayed hypersensitivity.
• T cells on contact with the antigens produce a
soluble protein – lymphokine.

29. MECHANISMS OF TYPE 4 HYPERSENSITIVITY
• When T cells primed to an antigen come in contact with the
same antigen for the second time the cell release
lymphokines.
• This activates macrophages to kill intra cellular bacteria.
• It involves:
 TUBERCULIN REACTION
• It is due to the interaction of sensitized T cells and
tuberculin bacterium.
• It is a delayed hypersensitivity.
 CONTACT DERMITITIS
• It is the inflammation of the skin due to contact with a
substances to which the person is allergic.

31. Some clinical examples:
• Contact dermatitis (poison ivy rash, for example)
• Temporal arthritis
• Symptoms of leprosy
• Symptoms of tuberculosis
• Transplant rejection

32. TYPE 5 HYPERSENSITIVITY
• It is caused by the interaction of antibodies with cell
surface antigen leading to stimulation of cells.
• While comparing with type 2 ,instead of stimulation
destruction of cell occurs.
• This phenomenon occurs in Graves disease.
• Stimulation of thyroid cells by TSH is another
example.