HUMORAL IMUNITY & CELLMEDIATED IMMUNITY
Humoral Immunity and Cell-mediated immunity
 Both types of immunity work in concert and are
interdependent
 Humoral immunity
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produces antibodies in response to extracellular
pathogens and toxins.
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Depends on antibody-producing B-cells.
 Cell-mediated immunity

responds to intracellular pathogens, transplanted tissues,
and cancer cells.

Depends on direct action of T-cytotoxic (Tc) cells
instead of antibodies.
Helper T lymphocytes function in both humoral and
cell-mediated immunity
 Combats pathogens that have already invaded cells.
 Key components are helper T cells (Th) and cytotoxic T cells
(Tc).
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These T cells mature in thymus and then migrate to
lymphoid organs (spleen and lymph nodes).
T cells respond only to antigenic epitopes displayed on
surfaces of body’s own cells.
Do not detect free antigens in body fluids

CD4 is a cell surface molecule displayed by T cells which enhances
the interaction between Th cells and antigen presenting cells (APC).

Helper T cells stimulate other lymphocytes by receiving and sending
cytokines.

When Th cell binds to an antigen presenting macrophage, the
macrophage releases interleukin-1 (a cytokine).

Interleukin-1 stimulates Th cell to release interleukin-2.
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Interleukin-2 stimulates the Th cells to grow and divide rapidly
resulting in the production of more Th cells and an increase in
supply of interleukin-2.

Because interleukin-2 and other cytokines secreted by the
increasing numbers of Th cells activate B cells, the humoral
response is enhanced.

Increased level of cytokines also increases cell-mediated response
by stimulating another class of T lymphocytes to differentiate into
cytotoxic T cells (effector cells).
The Humoral response
 Humoral response occurs when B-cells become activated by
the exposure of antigen to helper T cells.

The B cells differentiate into a clone of plasma cells that
will secrete antibodies.

Antibodies are most effective against pathogens
circulating in blood or lymph.
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Memory cells are also involved and form basis of
secondary immune response.
 Activation of B cells

Selective activation of B cells to produce plasma cells and
memory cells is actually a two-step process:
1. Binding of antigen on specific antigen-receptor on
surface of B cell.
2. Involves macrophages and Th cells. This step results in
production of plasma and memory cells.

macrophage phagocytize pathogens. Pieces of partially digested antigen
are presented on the surface of macrophage – APC

A Th cell with receptor specific for the presented antigen binds to the
antigen.

Th cell is now activated and proliferates to produce a clone of activated
Th cells specific for the presented antigen.

These activated Th cells secrete cytokines which stimulate B cells.

The B cells form clone of plasma cells.
 Each plasma cells (effector) then secretes antibodies for
the specific antigen.
 Each effector cells can produce a many as 2,000 antibodies
per second during its 4-5 day life span.
 Some antigens trigger humoral response without macrophage
or Th cells involvement. This response is weaker and no
memory is generated.
Cell-mediated immunity

cells destroy infected host cells

Host cells infected by viruses and other pathogens display
antigens on their surfaces.

Tc cells have specific receptors which recognize and bind to
antigen.

Tc receptor can bind to any body cell.
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When Tc cell binds to an infected cell, it releases perforin, a
protein that forms lesions in the infected cells membrane
causing cell lysis.
Cytotoxic T cells continue to live after destroying infected cell
and go on to kill other cells.
 Cytotoxic T cells also function to destroy cancer cells which
develop periodically in the body.
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Cancer cells possess distinctive markers not found in
normal cells. These markers are recognized by Tc cells as
non-self.
Cancer develops primarily in individuals with defective or
declining immune systems.
Memory cells function in secondary immune
responses
 Primary immune response = proliferation of lymphocytes to
form clones of effector cells specific to an antigen during
the body’s first exposure to the antigen.
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there’s lag time (5-10 days) between exposure and
maximum production of effector cells. The lymphocytes
selected by antigen are differentiating into effector T
cells and plasma cells during this lag period.
 Secondary immune response = occurs when body exposed to
a previously encountered antigen.
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Response faster and more prolonged than primary
response.
Antibodies are more effective at binding antigen.
 Ability to recognize previously encountered antigens known
as Immunologic memory.
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Based on memory cells produced during primary immune
response.
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Inactive during primary response. Long lived.
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When a previously encountered antigen enters body, it
rapidly activates memory cells to divide and form new
clones of effector cells and memory cells. These new
effector cells constitute the secondary immune response.
Types of immunity
Natural passive immunity
 Antibodies made in one individual are passed into another
individual of the same species.
 This only affords temporary protection, for, as the
antibodies do their job, or are broken down by the body's
natural processes, their number diminishes and protection is
slowly lost.
 For example, antibodies from a mother can cross the
placenta and enter her foetus. In this way they provide
protection for the baby until its own immune system is fully
functional.
 Passive immunity may also be conferred by colostrum (the
mother’s first milk), from which antibodies are absorbed in
the intestines of the baby.
Acquired passive immunity
 antibodies which have been made in one individual are
extracted and then injected into the blood of another
individual which may, or may not, be of the same species.
 For example, specific antibodies used for combating tetanus
and hepatitis B are cultured in horses and later injected into
Man.
 They act to prevent tetanus and hepatitis respectively. This
type of immunity is again short-lived – a matter of weeks
only.
Natural active immunity
 The body manufactures its own antibodies when exposed to
an infectious agent.
 Since memory cells produced on exposure to the first
infection are able to stimulate the production of massive
quantities of antibody, when exposed to the same antigen
again.
 This type of immunity is most effective and generally
persists for a long time - sometimes even for life.
Acquired active immunity
 This is achieved by injecting small amounts of antigen - the
vaccine - into the body of an individual.
 The whole process is called vaccination or immunisation. The
small dose of antigen is usually safe because the pathogen is
either killed or attenuated (= crippled).
 This ensures that the individual does not contract the disease
itself, but is stimulated to manufacture antibodies against the
antigen.
 Often a second, booster, injection is given and this stimulates a
much quicker production of antibody which is long lasting and
which protects the individual from the disease for a
considerable time.