Hypersensitivity reactions occur when the immune system responds in an exaggerated or inappropriate manner following contact with an antigen. There are four main types of hypersensitivity reactions: 1. Type I reactions are mediated by IgE antibodies and mast cells, causing immediate reactions like anaphylaxis. 2. Type II reactions involve IgG and IgM antibodies binding to antigens on a person's own cells, leading to cell damage or lysis. 3. Type III reactions involve immune complex deposition in tissues, complement activation, and inflammatory cell infiltration causing tissue damage. 4. Type IV delayed reactions are mediated by T cells and involve responses like contact dermatitis and tuberculin reactions occurring 1-3 days after

1. Lakhan.M.S
Hypersensitivity Reactions

2. Hypersensitivity
 Undesirable injurious consequences in the
sensitised host,following contact with specific
antigen.
 Generally the immune system is protective
 Protective mechanisms may result in severe
damages to tissues and may lead to death
 Severe damages may occur when the
immune system respond in exaggerated or
inappropriate form.

3.  Sensitising dose or Priming dose.
Initial contact with antigen-
sensitises Immune system-B & T
lymphocytes.
 Shocking dose
Subsequent contact with same
antigen-
HYPERSENSITIVITY REACTIONS.

4. Type of reaction Clinical Syndrome Mediators
Type I (IgE type) 1.Anaphylaxis
2.Atopy
IgE,histamine
Type 2 (Cytolytic &
Cytotoxic)
1.Thrombocytopeni
a
2.Agranulocytosis
3.Haemolytic
Anaemia
IgG IgM
Type 3 (Immune
Complex)
1.Arthus reaction
2.Serum Sickness
IgG IgM
Type 4 (Delayed type) 1.Tuberculin.
2.Contact
Dermatitis.
T cells

5. Type I Reactions
 SENSITISED INDIVIDUALS- antibodies are fixed
on surface of tissue cells-Mast cells & Basophils.
 On subsequent exposure
Antigen combines with cell fixed
antibody- release of Pharmacologically Active
Substances.
HYPERSENSITIVITY REACTIONS

6.  Two forms
 ANAPHYLAXIS –acute,fatal & systemic
 ATOPY – recurrent,non-fatal & localised

7. Exposure to allergen
Production of IgE Ab+
fix to mast cell
On Re-Exposure
Antigen-Antibody complex
on mast cell surface
Release Mediators Clinical manifestations of
anaphylaxis

8. Mediators
 Vasodilation and increased permeability
Histamine
Leukotriene
Prostaglandin
Neutral proteases
 Smooth muscle spasm
Histamine
Leukotriene
Prostaglandin
 Leukocyte extravasation
Cytokines (e.g. chemokines and TNF)
Leukotriene
Chemotactic factors for neutrophils and eosinophils

9. Type I – Examples
 Allergic asthma
 Allergic conjunctivitis
 Allergic rhinitis
 Angioedema
 Urticaria

10. ATOPY
 Familial,occurs spontaneously.
 Common antigens- Pollens,House dust & Food.
 Atopic individuals have higher levels of IgE and
eosinophils
 Mechanism of action- Similar to anaphylaxis but
reaction occurs at the site of entry and sensitising
dose not required.

11. Type I Hypersensitivity
 Prevention of type I hypersensitivity
 Identify and avoid allergens
 Identify food allergens by eliminating
suspected foods from diet
 Immunotherapy can help prevent allergic
reactions
 Administer a series of injections of dilute
allergen
 Must be repeated every two to three
years

12. Treatment of type I
hypersensitivity
 Administer drugs that counteract
inflammatory mediators
 Antihistamines neutralize histamine
 Treat asthma with a corticosteroid and a
bronchodilator
 Epinephrine neutralizes many
mechanisms of anaphylaxis
 Relaxes smooth muscle
 Reduces vascular permeability
 Severe asthma and anaphylactic shock
require emergency treatment

13. Treatment of Anaphylactic
Shock
1.Inj .Adrenaline (1:1000) 0.3-0.5 ml im.
2.Inj.Hydrocortisone 100-200 mg iv.
3.Inj.Pheniramine 45 mg im/iv.
4.IV fluids.

14. Type II Reactions
 Cytotoxic & Cytolitic
 Antibodies produced by the immune response
bind to antigens on the patient's own cell
surfaces.
 Causes
1.Phagocytosis of cell through opsonic
adherence.
2.Cytotoxicity by Natural Killer cells.
3.Lysis through activation of complement
system.

15.  Antigens can be
-Intrinsic ("self" antigen, innately part of patient's cells)
-Extrinsic (adsorbed onto the cells during exposure to foreign
antigen).
 These cells are recognized by macrophages or dendritic cells,
which act as antigen-presenting cells.
 This cause B cell response, where antibodies are produced
against foreign antigen

16. Examples
 Autoimmune Anaemia & Haemolytic disease of the
newborn.- Antierythrocyte antibody causes lysis of
red cells.
 Goodpasture's syndrome
Basement membrane(containing collagen type IV) in
the lung and kidney is attacked by our own antibodies
 Drug reactions-
Sedormid purpura
Other drugs Sulphonamides,Thiazide
diuretics,Quinidine also causes similar type of
purpura.

17. Other examples of Type II
 Pernicious anemia
 Immune thrombocytopenia
 Transfusion reactions
 Hashimoto's thyroiditis

18. Type III- Immune Complex Reactions
 Characterised by
1.Deposition of Antigen-Antibody complex in
tissue.
2. Activation of Complement
3.Infiltration of Polymorphonuclear leucocytes.
TISSUE DAMAGE
Antigen combines with Antibody
Producing Free floating Complex
Deposited in tissues
Immune-Complex Reactions

19. Type III
 Two types
-Arthus Reaction (Localised)
-Serum Sickness (Generalised)
Serum sickness- A single dose serves both as the
sensitising and shocking dose. –
Fever,Urticaria,Arthralgia,Lymphadenopathy,Sple
nomegaly.

20. Type III (Immune Complex–
Mediated) Hypersensitivity
 Caused by formation of immune complexes
 Can cause localized reactions
 Hypersensitivity pneumonitis
 Glomerulonephritis
 Hypersensitivity pneumonitis
 Inhalation of antigens into lungs stimulates
antibody production
 Subsequent inhalation of the same antigen
results in formation of immune complexes
 Activates complement

21. Type III (Immune Complex–
Mediated) Hypersensitivity
 Can cause systemic reactions
 Systemic lupus erythematosus
 Rheumatoid arthritis

22. Type IV Delayed or cell mediated
Reactions
 Mediated by sensitised T Lymphocytes
Contact with specific Antigen
Release Lymphokines
Effect on Macrophage,Leucocytes &
Tissue Cells.
 Occurs within 48-72 hours of antigen exposure.

23. Type IV Delayed or cell mediated
Reactions
 Two types
Tuberculin Type
Contact Dermatitis

24. Type IV
 The tuberculin response
 An injection of tuberculin beneath the skin
causes reaction in individual exposed to
tuberculosis or tuberculosis vaccine
 Used to diagnose contact with antigens of
M. tuberculosis
 No response when individual not
infected or vaccinated
 Red, hard swelling develops in
individuals previously infected or
immunized

26. Type V Stimulatory type
 Modification of Type II hypersensitivity reactions.
 Antigen-Antibody reaction enhances the activity
of affected cells- cell proliferation &
differentiation,instead of inhibition or killing.
Example
-Graves disease
presence of Long Acting Thyroid Stimulating
Antibody
-Mysthaenia Gravis

28.  Thank You