HYPERSENSITIVITY REACTION

NAME ABEERA ASIF

ID NO 13103
HYPERSENSITIVITY REACTION
• Hypersensitivity reactions are an overreaction of
the immune system to an antigen which would not
normally trigger an immune response.
• The antigen may be something which would in
most people be ignored peanuts, for example, or it
may originate from the body.
• In either case, the damage and clinical symptoms
result from the body’s response to the substance
rather than damage caused by the substance itself.
ANTIGEN
• “An antigen is a molecule that initiates the production of an antibody
and causes an immune response.”

• Antigens are large molecules of proteins, present on the surface of the

pathogen- such as bacteria, fungi viruses, and other foreign particles.
When these harmful agents enter the body, it induces an immune
response in the body for the production of antibodies.
 MAJOR HISTOCOMPATIBILITY PROTEIN

• The MHC genes are the most polymorphic genes in the human
genome, possessing many alleles for each gene. The MHC genes are
co-dominantly expressed so that an individual expresses the alleles
inherited from each parent.
• In addition, each MHC molecule is able to bind a wide variety of
different peptides, both self-peptides and foreign peptides. There are
two classes of MHC molecules: MHC-I and MHC-II.

• MHC-I molecules present epitopes to T8-lymphocytes.

• MHC-II molecules presents epitopes to T4-lymphocytes .
MHC molecules are important components of the immune system
because they allow T lymphocytes to detect cells, such as macrophages,
that have ingested infectious microorganisms
ANTIGEN PRESENTING CELL FUNCTION
TYPES OF HYPERSENSTIVITY REACTION
• TYPE 1
• The anaphylactic response is mediated by IgE antibodies that are produced
by the immune system in response to environmental proteins (allergens)
such as pollens, animal dangers, or dust mites.

• In Type 1 hypersensitivity reactions mast-cell activation is induced by

secretion of IgE antibodies. Initial exposure to the antigen causes the
priming of Th2 cells, and their release of IL-4 causes the B cells to switch
their production of IgM to IgE antibodies which are antigen-specific.
• The IgE antibodies bind to mast cells and basophils, sensitising them to the
antigen.

• When the antigen enters the body again, it cross links the IgE bound to the
sensitised cells, causing the release of preformed mediators including
histamine, leukotrienes and prostaglandins.
• This leads to widespread vasodilation, bronchoconstriction, and increased
permeability of vascular endothelium.
Example of Type 1
Type I hypersensitivity reactions can be seen in bronchial asthma,
allergic rhinitis, allergic dermatitis, food allergy, allergic conjunctivitis,
and anaphylactic shock.

Anaphylaxis is a systemic response to an antigen, leading to

bronchoconstriction and vasodilation. This decline in oxygen
transportation and can lead to anaphylactic shock and possibly death. It
is usually treated with adrenaline
TYPE 2 HYPERSENSITIVITY REACTION

• Type 2 hypersensitivity, also known as cytotoxic hypersensitivity or

antibody-mediated hypersensitivity, is an immune response characterized
by the activation of antibodies that target and damage the body's own cells.
• This type of hypersensitivity is mediated by antibodies, particularly
immunoglobulin G (IgG) and, to a lesser extent, immunoglobulin M (IgM).
Target Cells:
The immune response targets specific cells or tissues in the body. These cells
or tissues express antigens that are recognized by antibodies as foreign or
abnormal.
• Antibody-Mediated Damage:
Antibodies, mainly IgG and IgM, are produced in response to specific
antigens on the surface of the body's cells. These antigens may be normal
components of the body or may be altered in some way.
• Antibody binding to antigens on cell surfaces can activate the complement
system, leading to the formation of membrane attack complexes that
damage cell membranes.
TYPE 2
• Antibody binding can trigger various mechanisms of cell
destruction, including:

• Complement Activation:
• Complement proteins are activated, leading to the formation of
membrane attack complexes that cause cell lysis.
• Opsonization:
• Antibody-coated cells are recognized by phagocytes, leading to
the phagocytosis and destruction of the target cells.
• Antibody-Dependent Cellular Cytotoxicity (ADCC):
Antibodies activate immune cells, such as natural killer (NK)
cells, to release cytotoxic substances that induce target cell
death.
EXAMPLE OF TYPE 2

• Hemolytic Transfusion Reaction: If blood from a mismatched blood

type is transfused, antibodies against the foreign blood group antigens can
lead to the destruction of red blood cells.

• Rh Incompatibility in Pregnancy: Rh-negative mothers carrying Rh-

positive fetuses may produce antibodies against fetal Rh antigens, leading to
hemolytic disease of the newborn.
TYPE 3
• These are also mediated by IgM and IgG antibodies that react with
soluble antigens forming antigen-antibody complexes.
• The complement system becomes activated and releases chemotactic
agents that attract neutrophils and cause inflammation and tissue
damage as seen in vasculitis and glomerulonephritis.

• EXAMPLE
• Rheumatoid arthritis can occur when antigen-antibody complexes
circulate in the bloodstream end up lodging in the complex filtration
systems responsible for maintaining the levels of synovial fluids at
synovial joints. The lodged immune complexes can cause a local
inflammatory response, leading to stiffness and pain in affected joint
TYPE 4
• Type 4 hypersensitivity, also known as delayed-type
hypersensitivity (DTH) or cell-mediated hypersensitivity, is an
immune response that involves the activation of T lymphocytes
and occurs over a delayed period, typically 24 to 72 hours after
exposure to the antigen.
• This type of hypersensitivity is characterized by the involvement of
T cells and does not rely on antibodies.

• Type 4 hypersensitivity reactions are mediated by antigen-specific

activated T-cells. When the antigen enters the body, it is processed
by antigen-presenting cells and presented together with the MHC
II to a Th1 cell.

• If the T-helper cell has already been primed to that specific

antigen, it will become activated. Subsequently, it releases
chemokines to recruit macrophages and cytokines such as
interferon-γ to activate them.
Type 4

Activated macrophages release pro-inflammatory factors, leading to local

swelling, oedema, warmth, and redness.

EXAMPLE

Contact dermatitis can result from a wide variety of innocuous substances,

such as nickel, poison ivy, or household cleaning products. Because of the
delay in transporting Th1 cells to the site of infiltration, symptoms can
develop several days after initial exposure. Redness, itching, swelling, and
heat are all common.