HYPERSENSITIVITY

Mohamed Sajid

Guided by:
Dr. Hemalatha
 DEFINITION
• Hypersensitivity refers to the undesirable injurious consequences in a
sensitized host, following contact with specific antigen.

• Allergy refers to all immune processes harmful to the host – hypersensitivity

and autoimmunity.

• For induction of hypersensitivity reactions, the host should come in contact

with the allergen. This leads to priming of the appropriate B or T lymphocytes.
Called sensitizing or priming dose.

• Subsequent contact with allergen causes hypersensitivity reaction. Called

shocking dose.
 CLASSIFICATION
Hypersensitivity reactions are classified based on the time taken for the
sensitized host to develop clinical reactions on re-exposure to antigens –

• Immediate – Divided further into

• Anaphylaxis (Type 1)
• Cytotoxic (Type 2)
• Immune Complex Diseases (Type 3)

• Delayed (Type 4)
 DIFFERENCE BETWEEN IMMEDIATE AND
DELAYED HYPERSENSITIVITY REACTIONS
Immediate Hypersensitivity Delayed Hypersensitivity
Reaction Reaction
• Appears slowly but lasts longer.
• Appears and recedes rapidly.
• Antigen or hapten intradermally or with
• Induced by antigens or haptens by any Freund’s adjuvant or by skin contact.
route.
• Circulating antibodies may be absent
• Circulating antibodies present and and not responsible for reaction.
responsible for reaction.
• Cell mediated
• Antibody mediated
• Transfer with T cells or transfer factor.
• Passive transfer possible with serum.
• Difficult but long-lasting.
• Desensitization is easy but short-lived.
 TYPE 1 HYPERSENSITIVITY REACTION
(ANAPHYLACTIC)
They occur in two forms:
I. Anaphylaxis – Acute, potentially fatal, systemic form
• IgE dependent
• Induced by antigens and haptens.
• Clinical features: Smooth muscle contraction and increased vascular permeability
• Types: Cutaneous, Passive Cutaneous, Anaphylaxis in vitro
• Primary mediators: Histamine, Serotonin, Chemotactic factors, Enzymatic mediators
• Secondary mediators: Prostaglandins and leukotrienes, PAF
• Signs and Symptoms: Itching of scalp and tongue, skin flushing, bronchospasm, eventually
leading to acute hypotension, loss of consciousness and death
II. Atopy – Chronic, non-fatal, localized form
• Atopic sensitivity – caused by overproduction of IgE antibodies
• Symptoms: Conjunctivitis, rhinitis, GiT symptoms, dermatitis
TYPE 2 HYPERSENSITIVITY REACTION
(CYTOTOXIC)

These reactions involve a combination of

IgG antibodies with the antigenic
determinants on the surface of cells leading
to cytotoxic or cytolytic effects.

Examples – Lysis of red cells caused by

anti-erythrocyte antibodies in autoimmune
anemias, hemolytic disease of the newborn.

Stimulatory hypersensitivity is a modified

form of Type 2 hypersensitivity. It is also called
Type 5 hypersensitivity reaction.
 TYPE 3 HYPERSENSITIVITY REACTION
(IMMUNE COMPLEX DISEASES)
The damage is caused by antigen-antibody complexes.

They occur in two forms

1. Arthus reaction – Localized
• When rabbits were injected subcutaneously with horse serum, initial injections had no
effect but with later injections, intense local reaction consisting of edema, induration
and hemorrhagic necrosis.
• Tissue damage – formation of antigen-antibody precipitates causing complement
activation and release of inflammatory molecules, leading to increased vascular
permeability and neutrophil infiltration.

2. Serum Sickness – Systemic

• Pathogenesis: Immune complexes forms and deposits on the endothelial lining of
blood vessels in various parts of the body, causing inflammatory infiltration.
• A single injection acts as both the sensitizing dose and shocking dose.
• The clinical syndrome: Fever, lymphadenopathy, splenomegaly, arthritis, etc.
 TYPE 4 HYPERSENSITIVITY REACTION
(DELAYED HYPERSENSITIVITY)
• It is a cell mediated immune response which is usually provoked by microbial
infections or haptens like simple chemicals applies on the skin, evolve slowly and
will have mixed cellular reactions involving lymphocytes and macrophages.

• Reaction is induced by sensitized T cells which on contact with specific antigen,

release cytokines that produce biological effects on leucocytes, macrophages
and tissue cells.

• Cannot be transferred by serum but can be transferred by lymphocytes or transfer

factor.

• Two Types
1. Tuberculin (infection) type
2. Contact Dermatitis type
Tuberculin type
• When a small dose of tuberculin injected intradermally in an individual
sensitized to tuberculoprotein by prior infection or immunization – induration
and inflammatory reaction – within 48-72 hrs. No response in unsensitized
individual.
• Tuberculin test indicates state of delayed hypersensitivity.

Contact dermatitis type

• Results from skin contact with a variety of chemicals – metals, drugs or plant
allergens
• Mechanism: Langerhans’ cells of the skin capture locally applied hapten,
and migrates it to the draining lymph nodes where they present the
processed antigen along with MHC molecules to T cells. T cells travel to skin
site and release lymphokines. Leads to influx of eosinophilsnkn and cause
tissue damage.
THANK YOU