24 Lecture Presentation

CAMPBELL BIOLOGY: CONCEPTS & CONNECTIONS,
NINTH EDITION, GLOBAL EDITION

PowerPoint Lectures
Chapter 24
The Immune System
TAYLOR
SIMON
DICKEY
HOGAN
REECE
© 2018 Pearson Education Ltd.

Lecture by Edward J. Zalisko
Introduction
• Viruses can cause cancers.
• In the 1980s, scientists discovered that the
sexually transmitted human papillomavirus (HPV)
caused cervical and anal cancers.
• HPV vaccines are available.
• How long these vaccines last is not known.

Figure 24.0_1

Figure 24.0_2
Chapter 24: Big Ideas
Innate Immunity Adaptive Immunity
Disorders of the Immune

System
INNATE IMMUNITY

24.1 All animals have innate immunity
• Nearly everything in the environment teems with
pathogens, agents that cause disease.
• The immune system is the body’s system of
defenses against agents that cause disease.
• Innate immunity is a series of defenses that
• act immediately upon infection and
• are the same whether or not the pathogen has
been encountered before.
• Invertebrates rely solely on innate immunity.

24.1 All animals have innate immunity
• Vertebrate innate immunity includes
• barriers such as skin and mucous membranes,
• interferons that interfere with viral infections,
• neutrophils and macrophages (phagocytes),
• natural killer cells, which recognize and help kill
cancer cells and virus-infected cells, and
• a complement system, a group of proteins that
can act with other defense mechanisms.
Checkpoint question How do phagocytes
recognize pathogens?

Figure 24.1a
Innate external barriers

skin/exoskeleton, acidic environment,
secretions, mucous membranes, cilia
if external barriers breached
Innate internal defenses

phagocytic cells, natural killer cells,
defensive proteins,
inflammatory response

Figure 24.1b
Pathogen
Innate immune
cell 1
2
Vacuole
Lysosome
containing
enzymes
3
5
4

24.2 The inflammatory response disinfects
damaged tissue
• Tissue damage triggers the inflammatory
response, which can disinfect tissues and limit
further infection.
• Figure 24.2 shows the chain of events that occur
when a splinter has broken the skin, allowing
infection by bacteria.

Figure 24.2_1
Bacteria Splinter
Signaling Macrophage
Mast cell molecules
Capillary
Red blood cells Neutrophil
1 Tissue injury; signaling molecules are released

from mast cells and macrophages that cause
nearby capillaries to dilate.

Figure 24.2_2
Bacteria Splinter
molecules Neutrophil Movement
Mast cell
of fluid
Capillary
1 Tissue injury; signaling molecules are released 2 Capillaries widen and become leaky.
from mast cells and macrophages that cause Neutrophils migrate to the infected area.
nearby capillaries to dilate.

Figure 24.2_3
Bacteria Splinter
Mast cell
of fluid
Capillary Phagocytosis
1 Tissue injury; signaling molecules are released 2 Capillaries widen and become leaky. 3 Neutrophils digest bacteria and
from mast cells and macrophages that cause Neutrophils migrate to the infected area. cell debris at the site, and
nearby capillaries to dilate. the tissue heals.

Bacteria Splinter
Mast cell
of fluid
Capillary Phagocytosis
1 Tissue injury; signaling molecules are released 2 Capillaries widen and become leaky. 3 Neutrophils digest bacteria and
from mast cells and macrophages that cause Neutrophils migrate to the infected area. cell debris at the site, and
nearby capillaries to dilate. the tissue heals.
Checkpoint question How does a change in the

structure of capillaries support the function of the
inflammatory response?
ADAPTIVE IMMUNITY

24.3 The adaptive immune response counters
specific invaders
• Adaptive immunity (acquired immunity) is a set of
defenses, found only within vertebrates, that is
activated only after exposure to specific
pathogens.
• Unlike innate immunity, adaptive immunity differs
from individual to individual, depending on what
pathogens they have been previously exposed to.

24.3 The adaptive immune response counters
specific invaders
• Any molecule that elicits an adaptive immune
response is called an antigen.
• An antibody is an immune protein found in blood
plasma that attaches to one particular kind of
antigen and helps counter its effects.
• Infections and vaccinations trigger adaptive
immunity.
Checkpoint question Would a patient who received
an antivenom shot for a snake bite have lifelong
immunity to that venom?

Figure 24.3
Innate external barriers

skin, acidic environment, secretions,
• Rapid response mucous membranes, cilia
• Recognize broad
ranges of pathogens if external barriers breached
• No “memory” Innate internal defenses
phagocytic cells, natural killer cells,
defensive proteins,
inflammatory response
if innate defenses don’t
clear infection
• Slower response
• Recognize specific Adaptive responses (lymphocytes)
pathogens
• Have “memory” Defense against Defense against
pathogens in pathogens inside
body fluids body cells
24.4 The lymphatic system becomes a crucial
battleground during infection
• The lymphatic system
• is involved in innate and adaptive immunity and
• consists of a branching network of
• lymphatic vessels, which collect fluid from body
tissues and return it as lymph to the blood,
• lymph nodes, little round organs packed with
macrophages and lymphocytes, and
• lymph, which is similar to the interstitial fluid that
surrounds body cells but contains less oxygen and
fewer nutrients.

24.4 The lymphatic system becomes a crucial
battleground during infection
• Lymph organs are packed with white blood cells
that fight infections.
• The lymphatic system thus has two main functions:
1. to return tissue fluid back to the circulatory
system and
2. to fight infection.
Checkpoint question What might be the main
symptom of blockage of a large lymphatic vessel?

Figure 24.4
Organs
Adenoid Lymphatic ducts

that drain into veins Lymph node
Tonsils Lymph
Lymph nodes Masses of
lymphocytes and
Thymus Lymphatic macrophages
vessels
Valve
Spleen Lymphatic vessel
Blood capillary
Tissue cells
Interstitial
Appendix fluid
Bone
marrow
Lymph
Lymphatic
capillary

Figure 24.4_1
Organs
Adenoid
Lymphatic ducts
Tonsils that drain into veins
Lymph nodes
Thymus
Lymphatic
vessels
Spleen
Appendix
Bone
marrow

Figure 24.4_2
Lymph node
Lymph
Masses of
lymphocytes and
macrophages
Valve
Lymphatic vessel
Blood capillary
Tissue cells
Interstitial fluid
Lymph
Lymphatic
capillary
24.5 Lymphocytes mount a dual defense
• Lymphocytes originate from stem cells in the bone
marrow.
• B lymphocytes, or B cells, continue developing in
bone marrow.
• T lymphocytes, or T cells, develop further in the
thymus.
• By mounting a dual defense, B and T cells defend
against infections in body fluids and inside cells.

Figure 24.5a
Stem cell
Bone
marrow
Via
blood
Immature
lymphocytes
Thymus
Antigen
receptors
Via
blood
B cell T cell
Final maturation
of B and T cells in a
lymphatic organ
Lymph
nodes,
spleen,
and other
lymphatic
organs
Humoral immune response: Cell-mediated immune response:

action against free-floating antigens action against infected cells
Figure 24.5a_1
Stem cell
Bone
marrow
Via
blood
Immature
lymphocytes
Thymus
Antigen
receptors
B cell T cell
Figure 24.5a_2
Antigen
receptors
Via
blood
B cell T cell
Final maturation
of B and T cells in a
lymphatic organ
Lymph
nodes,
spleen,
and other
lymphatic
organs
Humoral Cell-mediated
immune response: immune response:
action against free- action against
floating antigens infected cells
Figure 24.5b
Antigen receptor Different antigen

on the cell surface receptors
The diversity of
+ + + = lymphocytes in
an individual
This cell might This cell might This cell might Millions of lymphocytes
recognize a recognize a recognize one of with different antigen
single antigen different antigen several antigens receptors
on the mumps on the mumps on the bacterium
virus virus causing tetanus

24.5 Lymphocytes mount a dual defense
• Millions of kinds of B cells and T cells, each with
different membrane receptors, wait in the
lymphatic system, where they may respond to
invaders.
• One of the two adaptive responses, produced by B
cells, is the humoral immune response, which
defends primarily against bacteria and viruses
present in body fluids.
• The second type of adaptive immunity, produced by
T cells, is the cell-mediated immune response,
which defends against infections inside body cells.

Figure 24.UN02
The humoral immune response:
makes which bind to
B cell
Antibodies Antigens in
body fluid
The cell-mediated immune response:
Cytotoxic Infected
T cell body cell
Self-nonself complex

24.6 Antigen receptors and antibodies bind to
specific regions on an antigen
• Both the humoral and cell-mediated immune
responses are initiated when lymphocytes
recognize antigens.
• B cells bind antigens directly.
• T cells require an additional step for recognition.
• The site on the antigen that antibodies and antigen
receptors bind to is the epitope.
• The specific region on an antigen receptor or
antibody that recognizes an epitope is the antigen-
binding site.

Antigen-binding
Two different sites
antibodies
Epitopes
Antigen
Pathogen
surface
Checkpoint question Why is it inaccurate to refer

to a pathogen, such as a virus, as an antigen?
24.7 VISUALIZING THE CONCEPT: Clonal
selection mobilizes defensive forces against
specific antigens
• The humoral and cell-mediated immune responses
both defend against a wide variety of antigens
through a process known as clonal selection.
• When an antigen enters the body, it activates only a
small subset of lymphocytes that have receptors
specific for the antigen.
• The selected cells multiply into clones of short-lived
effector cells specialized for defending against that
antigen and into memory cells, which confer long-
term immunity.

Figure 24.7_1
The Steps of Clonal Selection

Antigen
Antigen binds to
a B cell that has
corresponding Antigen
antigen receptors. receptors
B cell B cells

Figure 24.7_2

Antigen
Antigen binds to
a B cell that has
B cell B cells
Selected B cell divides,
forming identical cells
specialized against the
antigen that triggered the
response.
Clone of B cells

Figure 24.7_3

Antigen
Antigen binds to
a B cell that has
B cell B cells
response.
Antibodies
Clone of B cells
Antigen
Some B cells
differentiate into
effector cells that
secrete antibodies into
blood and lymph.
Effector B cells
Antigens bound by antibodies are

marked for destruction by innate
defenses.
Macrophage

Figure 24.7_4

Antigen
Antigen binds to
a B cell that has
B cell B cells
response.
Antibodies
Some B cells differentiate
into memory cells, which Clone of B cells
remain in the lymph Antigen
nodes.
Some B cells
differentiate into
effector cells that
blood and lymph.
Memory Effector B cells

cells

marked for destruction by innate
defenses.
Macrophage

Figure 24.7_5

Antigen
Antigen binds to
a B cell that has
B cell B cells
response.
Antibodies
Some B cells differentiate
into memory cells, which Clone of B cells
remain in the lymph Antigen
nodes.
Some B cells
differentiate into
effector cells that
blood and lymph.
Memory Effector B cells

cells
Memory cells Effector cells
help activate the are highly effective marked for destruction by innate
immune system upon at combating an defenses.
subsequent infection existing infection
Macrophage
last for decades last for only 4 or 5
days before dying off

24.8 The primary and secondary responses
differ in speed, strength, and duration
• The first exposure to an antigen results in the
primary immune response.
• In a second exposure, memory cells initiate a
faster, stronger, and more prolonged secondary
immune response.
• The secondary immune response, like the primary,
activates both effector cells and memory cells.
Checkpoint question What is the immunological
basis for referring to certain diseases, such as
chicken pox, as childhood diseases?

Figure 24.8a
Second
exposure
to antigen
Memory B cells produced by the primary response
Antibodies
Clone of effector B cells

secreting antibodies Clone of memory cells
Figure 24.8b
Second exposure
to antigen X, Secondary immune
first exposure response to
to antigen Y antigen X
Antibody concentration
First exposure
to antigen X
Primary immune Primary immune

response to response to
antigen X antigen Y
Antibodies Antibodies
to X to Y
0 7 14 21 28 35 42 49 56
Time (days)

24.9 CONNECTION: Herd immunity prevents
the outbreak of infectious disease
• When most people in a population are vaccinated,
a disease cannot spread.
• This community protection, called herd immunity,
is the rationale behind state-mandated
vaccinations for children in public schools.

Checkpoint question Herd immunity can only work
effectively if the level of immunization to a specific
pathogen is maintained at _____% or higher.
24.10 The structure of an antibody matches
its function
• Antibodies do not kill pathogens. Instead,
antibodies mark a pathogen by combining with it to
form an antigen-antibody complex.
• An antibody has antigen-binding sites that bind to
specific antigens.
• When bound to antigens on the surface of foreign
cells, antibodies assist innate responses in
eliminating the invader.

Figure 24.10a
Pathogen
Antigen-binding
sites
Polypeptide
chains
Antigen
Antibody
Antigen-binding site
Figure 24.10b
Binding of antibodies to antigens
inactivates antigens by
Agglutination of Activation of the

Neutralization complement system
microbes
Bacteria Complement
Virus molecule
Bacterium Foreign cell Hole
Enhances Leads to
Phagocytosis Cell lysis
Macrophage
Animation: Antibodies

24.11 SCIENTIFIC THINKING: Scientists
measure antibody levels to look for waning
immunity after HPV vaccination
• Several vaccines have been developed to promote
active immunity before individuals come into
contact with cancer-causing strains of HPV.
• Scientists cannot predict if or when an HPV
vaccine’s effectiveness will decrease.

24.11 SCIENTIFIC THINKING: Scientists
measure antibody levels to look for waning
immunity after HPV vaccination
• To measure long-lasting antibody production
against HPV, scientists designed and carried out
two long-term studies.
• Figure 24.11 provides data on the levels of two
HPV-specific antibodies—anti-HPV-16 and anti-
HPV-18—in the blood of individuals vaccinated
with Gardasil (magenta bars) or Cervarix (blue
bars).

Figure 24.11
Anti-HPV-16 Anti-HPV-18
antibodies antibodies
Percentage of vaccinated individuals
measured measured
with measurable antibodies 100
90
80
70
Gardasil
60
50 Cervarix
40
30
20
10
0
5 9.4 5 9.4
Number of years after vaccination
Data from S-E. Olsson et al., Induction of immune memory following administration of
a prophylactic quadrivalent human papillomavirus (HPV) types 6/11/16/18 L1 virus-like
particle (VLP) vaccine, Vaccine 25: 3931–4939 (2007); P. S. Naud et al., Sustained
efficacy, immunogenicity, and safety of the HPV-16/18 AS04-adjuvanted vaccine: final
analysis of a long-term follow-up study up to 9.4 years post-vaccination, Human
Vaccines Immunotherapeutics 10: 2147–62 (2014).
Checkpoint question Based on the data in the
graph, does it seem likely that either vaccine will
require a booster in the future?
24.12 Helper T cells stimulate the humoral
and cell-mediated immune responses
• An antigen-presenting cell displays a foreign
antigen (a nonself molecule) and one of the
body’s own self proteins to a helper T cell.
• The helper T cell’s receptors recognize the self-
nonself complexes, and the interaction activates
the helper T cell.
• In turn, the helper T cell can activate cytotoxic T
cells of the cell-mediated response and B cells of
the humoral response.

Figure 24.12a
Microbe
Macrophage
1
Antigen from the microbe
(nonself molecule)
Self protein
Self-nonself
complex
T cell
receptor
3
2 Helper
T cell
4
Binding
site for the
Antigen-presenting self protein
cell Signaling molecules Binding site for
stimulate the the antigen
helper cell
Checkpoint question How can one helper T cell
stimulate both humoral and cell-mediated
immunity?
Video: T Cell Receptors

Animation: Helper T Cells

24.13 Cytotoxic T cells destroy infected body
cells
• Figure 24.13 illustrates how a cytotoxic T cell kills
an infected cell.
1. A cytotoxic T cell with a matching receptor binds
to an infected body cell. The T cell then
synthesizes several toxic proteins that act on the
bound cell, including one called perforin.

Figure 24.13_1
1 A cytotoxic T cell binds

to an infected cell.
Self-nonself
complex
Foreign
Infected antigen
cell
Perforin
Cytotoxic
molecule
T cell

cells
• Figure 24.13 illustrates how a cytotoxic T cell kills
an infected cell.
1. A cytotoxic T cell with a matching receptor binds
to an infected body cell. The T cell then
synthesizes several toxic proteins that act on the
bound cell, including one called perforin.
2. Perforin is discharged from the T cell and
attaches to the infected cell’s plasma membrane,
forming pores in it. T cell enzymes, which enter
the infected cell by endocytosis, break down
proteins.

Figure 24.13_2
1 A cytotoxic T cell binds 2 Perforin forms holes in the

to an infected cell. infected cell’s membrane,
and enzymes trigger cell
Self-nonself death.
complex
A hole
Foreign forming
Infected antigen
cell
Perforin
Cytotoxic
molecule
T cell Enzymes

cells
3. The breakdown of proteins kills the infected cell.
The death of the infected cell deprives the
pathogen of a place to multiply and also exposes
the contents of the infected cell to circulating
antibodies, which mark the released antigens for
disposal.
4. The cytotoxic T cell may move on to destroy other
cells infected with the same pathogen.

Figure 24.13_3
1 A cytotoxic T cell binds 2 Perforin forms holes in the 3 The infected cell
to an infected cell. infected cell’s membrane, dies.
Self-nonself death.
complex
A hole
Foreign forming
Infected antigen
cell
Perforin
Cytotoxic
molecule
T cell Enzymes

Figure 24.13_4
1 A cytotoxic T cell binds 2 Perforin forms holes in the 3 The infected cell
to an infected cell. infected cell’s membrane, dies.
Self-nonself death.
complex
A hole
Foreign forming
Infected antigen
cell
Perforin
Cytotoxic
molecule
T cell Enzymes
4 Cytotoxic T cell
can destroy other
infected cells.

Animation: Cytotoxic T Cells

24.14 CONNECTION: HIV destroys helper T
cells, compromising the body’s defenses
• AIDS (acquired immunodeficiency syndrome),
results from infection by HIV, the human
immunodeficiency virus.
• Although HIV can infect a variety of cells, it most
often attacks helper T cells (Figure 24.14A).

Figure 24.14a
Human helper T cell

HIV
Colorized TEM 7,000×

24.14 CONNECTION: HIV destroys helper T
cells, compromising the body’s defenses
• Immune system impairment makes AIDS patients
susceptible to cancers and opportunistic
infections.
• Since the AIDS epidemic was first recognized in
1981, the disease has killed nearly 39 million
people worldwide.
• Although AIDS is currently incurable, anti-HIV
drugs can slow HIV reproduction and the progress
of AIDS for years, allowing most patients to lead
normal lives.

Total
number
people
with HIV
Percent of
HIV-positive
adults receiving
antiviral medication Indonesia Nigeria India USA Brazil Malawi UK
8% 21% 37% 37% 41% 51% 91%
Checkpoint question What effect would HIV have

on innate immunity?
Animation: HIV Reproductive Cycle

24.15 EVOLUTION CONNECTION: The rapid
evolution of HIV complicates AIDS treatment
• As HIV reproduces, mutations occur, some of
which can generate new strains of the virus.
• The virus mutates at a very high rate during
replication because reverse transcriptase does not
have an editing function to correct mistakes.
• Some of these mutated viruses are less susceptible
to destruction by the immune system and survive,
proliferate, and mutate further.
Checkpoint question How is HIV able to mutate at
such a high rate?

24.16 The immune system depends on our
molecular fingerprints
• The ability of lymphocytes to recognize the body’s
own molecules—to distinguish self from nonself—
enables our adaptive immune response to battle
foreign invaders without harming healthy cells.
• Each person’s cells have a unique collection of self
proteins on the surface.
• More than a dozen genes contain information for
producing major histocompatibility complex
(MHC) molecules, the main self proteins.

24.16 The immune system depends on our
molecular fingerprints
Checkpoint question In what sense is a cell’s set
of MHC surface markers analogous to a
fingerprint?

DISORDERS OF THE IMMUNE SYSTEM

24.17 CONNECTION: Immune system
disorders result from self-directed or
underactive responses
• In autoimmune disorders, the immune system
targets self molecules.
• In immunodeficiency disorders, immune
components are lacking and frequent infections
occur.
Checkpoint question Would you expect a patient
with SCID to develop type 1 diabetes? Explain.

Figure 24.17

24.18 CONNECTION: Allergies are
overreactions to certain environmental
antigens
• Allergies are hypersensitive (exaggerated)
responses to otherwise harmless antigens in the
environment.
• Antigens that cause allergies are called allergens.
• Antihistamines interfere with histamine’s action
and give temporary relief from an allergy.
• Symptoms of an allergy result from a two-stage
reaction sequence outlined in Figure 24.18.

Figure 24.18
Sensitization: Initial exposure to an allergen Later exposure to the same allergen
Effector
B cell
Mast
cell
Allergen
Histamine
1 An allergen (pollen grain) 2 B cells make 3 Antibodies 4 The allergen binds 5 Histamine is
enters the bloodstream. antibodies. attach to a to antibodies on released, causing
mast cell. a mast cell. allergy symptoms.

Figure 24.18_1
Sensitization: Initial exposure to an allergen
Effector
B cell
Mast
cell
Allergen
Histamine
1 An allergen (pollen grain) 2 B cells make 3 Antibodies
enters the bloodstream. antibodies. attach to a
mast cell.

Figure 24.18_2
Later exposure to the same allergen
4 The allergen binds 5 Histamine is

to antibodies on released, causing
a mast cell. allergy symptoms.

You should now be able to
1. Describe the risks and prevention of HPV
infections.
2. Describe the nature of innate defenses of
invertebrates and vertebrates.
3. Describe the steps of the inflammatory
response.
4. Describe the specific nature of adaptive immune
system responses.
5. Describe the structure and functions of the
lymphatic system.

6. Describe the development and functions of B
lymphocytes and T lymphocytes
7. Describe the nature of antigens. Explain how an
antigen and an antibody interact.
8. Describe the process of clonal selection.
9. Compare a primary immune response to a
secondary immune response.
10. Explain how herd immunity prevents the spread
of disease.

11. Explain how the structure of an antibody
matches its functions.
12. Explain how scientists can predict if or when a
vaccine’s effectiveness will decrease.
13. Describe the specific functions of helper T cells
and how they interact with other cells.
14. Explain how cytotoxic T cells destroy infected
body cells.
15. Explain how HIV infects cells, multiplies, and
causes disease.

16.Explain why it has been difficult to develop a
successful treatment for AIDS.
17.Explain how the immune system identifies the
body’s own molecules and how this system
complicates organ transplantations.
18.Describe how the malfunction or failure of the
immune system can cause disease.
19.Explain why allergies occur and what causes
anaphylactic shock.

Figure 24.UN01

Figure 24.UN03
Body’s
defenses
include
(a) (b)
is present found in is present found in
vertebrates and only after

at birth vertebrates
invertebrates exposure
produced by cells called
Lymphocytes
include
(c) (d) (e)
stimulate
poke
secrete responsible for responsible for
“holes” in
humoral cell-mediated
(f) (g)
immune response immune response

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CAMPBELL BIOLOGY: CONCEPTS & CONNECTIONS,

NINTH EDITION, GLOBAL EDITION

© 2018 Pearson Education Ltd.

© 2018 Pearson Education Ltd.

© 2018 Pearson Education Ltd.

Innate Immunity Adaptive Immunity

Disorders of the Immune

© 2018 Pearson Education Ltd.

© 2018 Pearson Education Ltd.

© 2018 Pearson Education Ltd.

Innate external barriers

if external barriers breached

Innate internal defenses

© 2018 Pearson Education Ltd.

© 2018 Pearson Education Ltd.

© 2018 Pearson Education Ltd.

Red blood cells Neutrophil

1 Tissue injury; signaling molecules are released

© 2018 Pearson Education Ltd.

Red blood cells Neutrophil

© 2018 Pearson Education Ltd.

Red blood cells Neutrophil

© 2018 Pearson Education Ltd.

Red blood cells Neutrophil

Checkpoint question How does a change in the

© 2018 Pearson Education Ltd.

© 2018 Pearson Education Ltd.

© 2018 Pearson Education Ltd.

Innate external barriers

© 2018 Pearson Education Ltd.

© 2018 Pearson Education Ltd.

Adenoid Lymphatic ducts

© 2018 Pearson Education Ltd.

© 2018 Pearson Education Ltd.

© 2018 Pearson Education Ltd.

Humoral immune response: Cell-mediated immune response:

Antigen receptor Different antigen

© 2018 Pearson Education Ltd.

© 2018 Pearson Education Ltd.

The humoral immune response:

makes which bind to

© 2018 Pearson Education Ltd.

© 2018 Pearson Education Ltd.

Checkpoint question Why is it inaccurate to refer

© 2018 Pearson Education Ltd.

The Steps of Clonal Selection

© 2018 Pearson Education Ltd.

The Steps of Clonal Selection

© 2018 Pearson Education Ltd.

The Steps of Clonal Selection

Antigens bound by antibodies are

© 2018 Pearson Education Ltd.

The Steps of Clonal Selection

Memory Effector B cells

Antigens bound by antibodies are

© 2018 Pearson Education Ltd.

The Steps of Clonal Selection

Memory Effector B cells