Full Immunity Material

CAMPBELL BIOLOGY IN FOCUS
URRY • CAIN • WASSERMAN • MINORSKY • REECE
35
The Immune
System
Lecture Presentations by
Kathleen Fitzpatrick and
Nicole Tunbridge,
Simon Fraser University
© 2016 Pearson Education, Inc. SECOND EDITION

Overview: Recognition and Response
 Pathogens, agents that cause disease, infect a

wide range of animals, including humans
 The immune system enables an animal to avoid or
limit many infections
 All animals have innate immunity, a defense that is
active immediately upon infection
 Vertebrates also have adaptive immunity
© 2016 Pearson Education, Inc.

Figure 35.1

 Innate immunity includes barrier defenses
 A small set of receptor proteins bind molecules or
structures common to viruses, bacteria, or other
microbes
 Binding an innate immune receptor activates
internal defensive responses to a broad range of
pathogens

 Adaptive immunity, or acquired immunity, develops
after exposure to agents such as microbes, toxins,
or other foreign substances
 It involves a very specific response to pathogens

Figure 35.2
Pathogens
(such as bacteria,
fungi, and viruses)
INNATE IMMUNITY Barrier defenses:

(all animals) Skin
• Recognition of traits shared Mucous membranes
by broad ranges of Secretions
pathogens, using a small
set of receptors Internal defenses:
Phagocytic cells
• Rapid response Natural killer cells
Antimicrobial proteins
Inflammatory response
ADAPTIVE IMMUNITY Humoral response:

(vertebrates only) Antibodies defend against
• Recognition of traits infection in body fluids.
specific to particular
pathogens, using a vast Cell-mediated response:
array of receptors Cytotoxic cells defend
against infection in body cells.
• Slower response
Concept 35.1: In innate immunity, recognition and
response rely on traits common to groups of
pathogens
 Innate immunity is found in all animals and plants
 In vertebrates, innate immunity is an immediate
response to infections and serves as the foundation
of adaptive immunity

Innate Immunity of Invertebrates
 Insects rely on their exoskeleton as a physical

barrier against infection
 In the digestive system, the enzyme lysozyme
breaks down bacterial cell walls, protecting against
pathogens ingested along with food
 Immune cells of insects recognize pathogens by
binding to molecules specific to viruses or
microorganisms
 Each recognition protein of insects recognizes a
broad class of pathogens

 Hemocytes circulate within hemolymph and carry
out phagocytosis, the ingestion and breakdown of
foreign substances including bacteria
 Hemocytes also release antimicrobial peptides that
disrupt the plasma membranes of fungi and bacteria

Figure 35.3
Pathogen Pseudopodia
surround
pathogens.
Pathogens
are engulfed
PHAGOCYTIC CELL by endocytosis.
Vacuole forms.
Vacuole
Lysosome
containing
enzymes
Vacuole and
lysosome fuse.
Pathogens are
destroyed.
Debris from
pathogens
released.
Innate Immunity of Vertebrates
 The immune system of mammals is the best

understood of the vertebrates
 Innate defenses include barrier defenses,
phagocytosis, and antimicrobial peptides
 Additional defenses are unique to vertebrates:
natural killer cells, interferons, and the inflammatory
response

Barrier Defenses
 Barrier defenses include the skin and mucous

membranes of the respiratory, urinary, and
reproductive tracts
 Mucus traps and allows for the removal of microbes
 Many body fluids including saliva, mucus, and tears
are hostile to many microbes
 The low pH of skin and the digestive system
prevents growth of many bacteria

Cellular Innate Defenses
 Pathogens entering the mammalian body are

subject to phagocytosis
 Phagocytic cells recognize groups of pathogens by
Toll-like receptors (TLRs)
 Each mammalian TLR binds to fragments of
molecules characteristic to a set of pathogens

Figure 35.4
EXTRACELLULAR
FLUID Lipopolysaccharide
Helper
protein Flagellin
TLR4
PHAGOCYTIC CELL
TLR5
CpG DNA
TLR9
Innate immune
VESICLE responses
dsRNA
TLR3

 There are two main types of phagocytic cells in
mammals
 Neutrophils circulate in the blood and are attracted
by signals from infected tissues
 Macrophages are found throughout the body

 Two additional types of cells with roles in innate
defense
 Dendritic cells stimulate development of adaptive
immunity in cells that contact the environment (such
as skin)
 Eosinophils discharge destructive enzymes

 Cellular innate defenses in vertebrates also involve
natural killer cells
 These circulate through the body and detect
abnormal cells
 They release chemicals leading to cell death,
inhibiting the spread of virally infected or cancerous
cells
 Many cellular innate defenses involve the lymphatic
system

Antimicrobial Peptides and Proteins
 In mammals, pathogen recognition triggers release

of peptides and proteins that attack pathogens or
impede their reproduction
 Interferons provide innate defense, interfering with
viruses and helping activate macrophages
 The complement system consists of about 30
proteins that are activated by substances on
microbe surfaces
 Activation can lead to lysis of invading cells

Inflammatory Response
 The inflammatory response, such as pain and

swelling, is brought about by molecules released
upon injury of infection
 Activated macrophages and neutrophils release
cytokines, signaling molecules that modulate the
immune response and promote blood flow to the
site of injury or infection
 Mast cells release histamine, which triggers blood
vessels to dilate and become more permeable

 Enhanced blood flow to the site helps deliver
antimicrobial peptides
 This results in an accumulation of pus, a fluid rich in
white blood cells, dead pathogens, and cell debris
from damaged tissues

Figure 35.5
Pathogen Splinter
Movement
of fluid
Macro-
Signaling
Mast phage
molecules
cell
Capillary Phagocytosis
Red blood cells

Neutrophil
Histamines and cytokines Antimicrobial Neutrophils
released. Capillaries peptides enter digest pathogens
dilate. tissue. Neutrophils and cell debris.
are recruited. Tissue heals.

 Inflammation can be either local or systemic
(throughout the body)
 Fever is a systemic inflammatory response
triggered by substances released by macrophages
 Septic shock is a life-threatening condition caused
by an overwhelming inflammatory response
 Chronic inflammation can also threaten human
health

Evasion of Innate Immunity by Pathogens
 Adaptations have evolved in some pathogens that

enable them to avoid destruction by phagocytic cells
 The outer capsule of some bacteria interferes with
molecular recognition
 Tuberculosis (TB) resists breakdown within
lysosomes after being engulfed by a host cell

Concept 35.2: In adaptive immunity, receptors
provide pathogen-specific recognition
 The adaptive response relies on two types of
lymphocytes, or white blood cells
 Lymphocytes that mature in the thymus above the
heart are called T cells, and those that mature in
bone marrow are called B cells

Figure 35.UN01
Antigen
receptors
Mature B cell Mature T cell

 Antigens are substances that can elicit a response
from a B or T cell
 Recognition occurs when a B or T cell binds to an
antigen, via an antigen receptor
 The immune system produces millions of different
antigen receptors, but the receptors on a single B
cell or T cell are all identical to one another
 The small accessible part of an antigen that binds to
an antigen receptor is called an epitope

Antigen Recognition by B Cells and Antibodies
 Each B cell antigen receptor is a Y-shaped

molecule with two identical heavy chains and two
identical light chains
 The constant (C) regions of the chains vary little
among B cells, whereas the variable (V) regions
differ greatly
 Together, the V regions of the heavy and light
chains form an antigen-binding site

Figure 35.6
Antigen- Antigen-
binding binding site
site
Disulfide
bridge
Variable
regions
B cell Constant
antigen regions
receptor Light C C
chain Transmembrane
region
Heavy Plasma
chain membrane
B cell Cytoplasm of B cell
 Binding of a B cell antigen receptor to an antigen is
an early step in B cell activation
 This gives rise to cells that secrete a soluble form of
the protein called an antibody or immunoglobulin
(Ig)
 Secreted antibodies are similar to B cell receptors
but are not membrane bound
 The antibodies, rather than B cells themselves,
defend against pathogens

Animation: Antibodies

Figure 35.7
Antigen Antibody
receptor
B cell
Antigen Epitope
Pathogen
(a) B cell antigen receptors and antibodies
Antibody C
Antibody A
Antibody B
Antigen
(b) Antigen receptor specificity

Figure 35.7-1
Antigen Antibody
receptor
B cell
Antigen Epitope
Pathogen
(a) B cell antigen receptors and antibodies

Figure 35.7-2
Antibody C
Antibody A
Antibody B
Antigen
(b) Antigen receptor specificity

Antigen Recognition by T Cells
 Each T cell receptor consists of two different

polypeptide chains (called α and β)
 The tips of the chain form a variable (V) region; the
rest is a constant (C) region
 The V regions of the α and β chains together form
an antigen-binding site

Figure 35.8
Antigen-
binding
site
T cell Variable
antigen V V regions
receptor
Constant
C C regions
Transmembrane
Disulfide region
bridge
a chain b chain
Plasma
membrane
T cell Cytoplasm of T cell
 T cells bind only to antigen fragments displayed or
presented on a host cell
 MHC (major histocompatibility complex)
molecules are host proteins that display the antigen
fragments on the cell surface

 In infected cells, antigens are cleaved into smaller
peptides by enzymes
 MHC molecules bind and transport the antigen
fragments to the cell surface, a process called
antigen presentation
 A T cell can then bind both the antigen fragment
and the MHC molecule
 This interaction is necessary for the T cell to
participate in the adaptive immune response

Figure 35.9
Displayed
antigen T cell
fragment
T cell antigen
MHC receptor
molecule
Antigen
fragment
Pathogen

Host cell
B Cell and T Cell Development
 The adaptive immune system has four major

characteristics
 Diversity of lymphocytes and receptors
 Self-tolerance; lack of reactivity against an animal’s
own molecules
 Proliferation of B and T cells after activation
 Immunological memory

Generation of B Cell and T Cell Diversity
 By combining variable elements, the immune

system assembles millions of different receptors
 The capacity to generate diversity is built into the
structure of Ig genes
 Many different chains can be produced from the
same gene by rearrangement of the DNA
 Rearranged DNA is transcribed and translated and
the antigen receptor formed

 For example, a receptor light-chain gene contains a
variable (V) segment, a joining (J) segment, and a
constant (C) segment
 The gene contains one C segment, 40 different V
segments, and 5 different J segments
 These can be combined in 200 different ways
 The number of heavy-chain combinations is even
greater

Figure 35.10
DNA of undifferentiated B cell
V37 V38 V39 V40 J1 J2 J3 J4 J5 Intron C
Recombination deletes DNA between

randomly selected V segment and J segment
DNA of differentiated B cell
V37 V38 V39 J5 Intron C
Functional gene
Transcription of permanently
rearranged, functional gene
pre-mRNA V39 J5 Intron C
RNA processing
mRNA Cap V39 J5 C Poly-A tail

V V
Translation V V
C C
Light-chain polypeptide V C C C
Antigen receptor
Variable Constant
region region B cell
Figure 35.10-1
DNA of
undifferentiated
B cell
V37 V38 V39 V40 J1 J2 J3 J4 J5 Intron C
DNA of Recombination deletes DNA between

differentiated randomly selected V segment and J segment
B cell
V37 V38 V39 J5 Intron C
Functional gene
Transcription of permanently
rearranged, functional gene

Figure 35.10-2
pre-mRNA V39 J5 Intron C
RNA processing
mRNA Cap V39 J5 C Poly-A tail

V V
Translation V V
C C
Light-chain
V C
polypeptide Antigen receptor C C
Variable Constant
region region B cell

Origin of Self-Tolerance
 Antigen receptors are generated by random

rearrangement of DNA
 As lymphocytes mature in bone marrow or the
thymus, they are tested for self-reactivity
 Some B and T cells with receptors specific for the
body’s own molecules are destroyed by apoptosis,
or programmed cell death
 The remainder are rendered nonfunctional

Proliferation of B Cells and T Cells
 In the body only a tiny fraction of antigen receptors

are specific for a given epitope
 In the lymph nodes, an antigen is exposed to a
steady stream of lymphocytes until a match is made
 This binding of a mature lymphocyte to an antigen
initiates events that activate the lymphocyte

 Once activated, a B or T cell undergoes multiple cell
divisions to produce a clone of identical cells (called
clonal selection)
 Some cells become short-lived activated effector
cells that act immediately against the antigen
 For B cells, the effector forms are plasma cells,
which secrete antibodies
 Long-lived memory cells give rise to effector cells if
the same antigen is encountered again

Animation: Role of B Cells

Figure 35.11
B cells that Antigen

Antigen
differ in
receptor
antigen
specificity
Antibody
Plasma cells Memory cells

Immunological Memory
 Immunological memory is responsible for long-term

protection against diseases, due to a prior infection
 The first exposure to a specific antigen represents
the primary immune response
 During this time, selected B and T cells give rise to
their effector forms
 In the secondary immune response, memory cells
facilitate a faster, stronger, and longer response
 Immunological memory can span many decades

Figure 35.12
Primary immune Secondary Primary immune
response to immune response response to
antigen A to antigen A antigen B
104
Antibody concentration
(arbitrary units)
103
Antibodies
to A
102 Antibodies
to B
101
100
0 7 14 21 28 35 42 49 56
Exposure Exposure to
to antigen A antigens A and B
Time (days)
Concept 35.3: Adaptive immunity defends against
infection of body fluids and body cells
 B and T lymphocytes produce a humoral immune
response and a cell-mediated immune response
 In the humoral immune response, antibodies help
neutralize or eliminate toxins and pathogens in the
blood and lymph
 In the cell-mediated immune response
specialized T cells destroy infected host cells

Helper T Cells: Activating Adaptive Immunity
 A type of T cell called a helper T cell triggers both

the humoral and cell-mediated immune responses
 To produce this response
 A foreign molecule must be bound by the antigen
receptor of the helper T cell
 An antigen must be displayed on the surface of an
antigen-presenting cell
 Antigen-presenting cells have class I and class II
MHC molecules on their surfaces

 Antigen-presenting cells are recognized based on
their class II MHC molecules
 Antigen receptors on the surface of helper T cells
bind to the antigen and the class II MHC molecule
 Signals are then exchanged between the two cells
 The helper T cell is activated, proliferates, and
forms a clone of helper T cells, which then activate
the appropriate B cells

Figure 35.13-s1
Antigen- Antigen
presenting fragment
cell
Pathogen
MHC
Antigen CD4
receptor
Helper T cell

Figure 35.13-s2
Antigen- Antigen
presenting fragment
cell
Pathogen
MHC
Antigen CD4
receptor
Cytokines
Helper T cell

Figure 35.13-s3
Antigen- Antigen
presenting fragment
cell Clone of
activated
Pathogen helper
T cells
MHC Cyto-
B cell toxic
CD4 T cell
Antigen
receptor
HUMORAL CELL-
Cytokines IMMUNITY MEDIATED
Helper T cell IMMUNITY

B Cells and Antibodies: A Response to Extracellular
Pathogens
 The humoral response is characterized by secretion
of antibodies by clonally selected B cells
 Activation of B cells involves helper T cells and
proteins on the surface of pathogens
 A single activated B cell gives rise to thousands of
identical plasma cells

Figure 35.14-s1
Antigen- Pathogen
presenting
cell
Antigen
fragment MHC
CD4
Antigen
receptor
Helper T cell

Figure 35.14-s2
Antigen- Pathogen
presenting
cell
B cell
Antigen
fragment MHC
CD4
Cytokines
Antigen
receptor
Activated
Helper T cell helper T cell

Figure 35.14-s3
Antigen- Pathogen
presenting
cell
B cell
Memory B cells
Antigen
fragment MHC
CD4
Cytokines
Antigen
receptor
Activated
Helper T cell helper T cell Plasma cells
Secreted
antibodies

 Antibodies do not kill pathogens; instead, they mark
pathogens for destruction
 In neutralization, antibodies bind to viral surface
proteins, preventing infection of a host cell
 Antibodies may also bind to toxins in body fluids
and prevent them from entering body cells

 Antigen-antibody complexes may bind to a
complement protein
 A cascade of subsequent events leads to formation
of a pore in the membrane of the foreign cell,
leading to its lysis

Figure 35.15
Antibody
Virus

 B cells can express five different forms (or classes)
of immunoglobulin (Ig) with similar antigen-binding
specificity but different heavy-chain C regions
 One type, the B cell antigen receptor, is membrane
bound
 The others are soluble and include those found in
blood, tears, saliva, and breast milk

Cytotoxic T Cells: A Response to Infected Host Cells
 Cytotoxic T cells are the effector cells in the cell-

mediated immune response
 Cytotoxic T cells recognize fragments of foreign
proteins produced by infected cells and possess an
accessory protein that binds to class I MHC
molecules
 The activated cytotoxic T cell secretes proteins that
disrupt the membranes of target cells and trigger
apoptosis

Animation: Cytotoxic T Cells

Figure 35.16-s1
Cytotoxic
T cell
CD8 Antigen
MHC receptor
Infected
cell
Antigen
fragment

Figure 35.16-s2
Cytotoxic Granzymes
T cell Perforin
molecules
CD8 Antigen
MHC receptor
Infected Pore
cell
Antigen
fragment

Figure 35.16-s3
Released
Cytotoxic Granzymes cytotoxic
T cell T cell
Perforin
molecules
CD8 Dying
Antigen infected cell
MHC receptor
Infected Pore
cell
Antigen
fragment

Summary of the Humoral and Cell-Mediated
Immune Responses
 Both the humoral and cell-mediated responses can
include primary and secondary immune responses
 Memory cells enable the secondary response

Figure 35.17
Humoral (antibody-mediated) Cell-mediated
immune response immune response
Antigen (1st exposure)

Stimulates
Taken in by
Gives rise to
Antigen-
presenting cell
Cytotoxic
B cell Helper T cell T cell
Memory
helper T cells
Antigen (2nd exposure)

Plasma Memory Memory Active
cells B cells cytotoxic T cells cytotoxic T cells
Secreted
antibodies Defend against Defend against intracellular
extracellular pathogens pathogens and cancer
Figure 35.17-1

Antigen (1st exposure)

Stimulates
Taken in by
Gives rise to
Antigen-
presenting cell
Cytotoxic

Figure 35.17-2

Stimulates
Gives rise to
Cytotoxic
Memory
helper T cells
Antigen (2nd exposure)

Plasma Memory Memory Active
cells B cells cytotoxic T cells cytotoxic T cells
Secreted
antibodies Defend against Defend against intracellular
extracellular pathogens pathogens and cancer

Active and Passive Immunity
 Active immunity occurs naturally when a pathogen

infects the body
 Passive immunity provides immediate, short-term
protection
 It is conferred naturally when antibodies cross the
placenta from mother to fetus or pass from mother
to infant in breast milk
 Both active and passive immunity can be induced
artificially

 Active immunity is induced when antigens are
introduced into the body in vaccines
 In this process of immunization, inactivated
bacterial toxins or weakened or killed pathogens
are introduced
 Passive immunity can be conferred artificially by
injecting antibodies into a nonimmune person

Antibodies as Tools
 Polyclonal antibodies, produced following exposure

to an antigen, are products of many different clones
of plasma cells, each specific for a different epitope
 Monoclonal antibodies are prepared from a single
clone of B cells grown in culture
 Monoclonal antibodies have provided the basis for
many recent advances in medical diagnosis and
treatment

Immune Rejection
 Cells transferred from one person to another can be

destroyed (rejected) by the recipient’s immune
defenses
 To minimize rejection, physicians use donor tissue
that closely matches the MHC molecules of the
recipient
 Recipients also take medicines that suppress their
immune responses

Disruptions in Immune System Function
 Although adaptive immunity protects against many

pathogens, it is not fail-safe

Allergies
 Allergies are exaggerated (hypersensitive)

responses to antigens called allergens
 In localized allergies such as hay fever, plasma
cells secrete antibodies specific for antigens on the
surface of pollen grains
 This triggers immune cells in connective tissue to
release histamine and other inflammatory chemicals
 Antihistamines block receptors for histamine and
diminish allergy symptoms

Figure 35.18
IgE
antibodies
Cross-linking
of IgE antibodies
triggers release of
Allergen histamine.
Mast (second
cell exposure)
Initial exposure
produces IgE
antibodies which
bind to mast cell
receptors.
On subsequent Histamine
exposure, IgE
antibodies bind Vesicle
allergen.
 An acute allergic response can lead to anaphylactic
shock, a life-threatening reaction
 Substances that can trigger anaphylactic shock in
allergic individuals include bee venom, penicillin,
peanuts, and shellfish
 People with these hypersensitivities often carry
epinephrine to counteract the allergic response

Autoimmune Diseases
 In individuals with autoimmune diseases, the

immune system targets certain molecules of the
body
 Autoimmune diseases include systemic lupus
erythematosus, rheumatoid arthritis, type 1
diabetes, and multiple sclerosis
 Genes, heredity, and environment all influence
susceptibility to autoimmune disorders

Figure 35.19

Immune System Avoidance
 Mechanisms to thwart immune responses have

evolved in pathogens
 A pathogen may alter how it appears to the immune
system by changing the epitopes it expresses
 Such changes are called antigenic variation
 This mechanism is seen in the parasite that causes
sleeping sickness and in the influenza virus

 Some viruses avoid an immune response by
infecting cells and then entering an inactive state
called latency
 The virus (such as herpes simplex) remains latent
until a stimulus reactivates it
 Stimuli include stress, fever, or menstruation

 Acquired immunodeficiency syndrome (AIDS) is
caused by HIV (human immunodeficiency virus),
which both attacks and escapes the immune system
 It infects helper T cells with high efficiency
 It escapes the immune system through its high
mutation rate, which reduces the ability of the
immune system to eliminate the infection
 It also can undergo latency

 People with AIDS (acquired immune deficiency
syndrome) are highly susceptible to infections and
cancers that a healthy immune system would
normally defeat
 Unprotected sex and transmission via HIV-
contaminated needles account for the majority of
HIV infections
 HIV cannot be cured, but drugs have been
developed to slow HIV replication and progression
to AIDS

Cancer and Immunity
 The frequency of certain cancers increases when

adaptive immunity is impaired
 15–20% of all human cancers involve viruses
 The immune system can act as a defense against
viruses that cause cancer and against cancer cells
that harbor viruses
 In 2006, a vaccine was released that acts against
human papillomavirus (HPV), a virus associated
with cervical cancer

Figure 35.UN02-1

Figure 35.UN02-2

Figure 35.UN02-3

Figure 35.UN03
Stem cell
Cell division and
gene rearrangement
Elimination of
self-reactive
B cells
Antigen
Clonal
selection
Formation of Antibody
activated cell
populations
Plasma cells
Memory B cells
Pathogen
Receptors bind to antigens


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CAMPBELL BIOLOGY IN FOCUS

URRY • CAIN • WASSERMAN • MINORSKY • REECE

© 2016 Pearson Education, Inc. SECOND EDITION

 Pathogens, agents that cause disease, infect a

© 2016 Pearson Education, Inc.

© 2016 Pearson Education, Inc.

© 2016 Pearson Education, Inc.

© 2016 Pearson Education, Inc.

INNATE IMMUNITY Barrier defenses:

ADAPTIVE IMMUNITY Humoral response:

© 2016 Pearson Education, Inc.

 Insects rely on their exoskeleton as a physical

© 2016 Pearson Education, Inc.

© 2016 Pearson Education, Inc.

 The immune system of mammals is the best

© 2016 Pearson Education, Inc.

 Barrier defenses include the skin and mucous

© 2016 Pearson Education, Inc.

 Pathogens entering the mammalian body are

© 2016 Pearson Education, Inc.

© 2016 Pearson Education, Inc.

© 2016 Pearson Education, Inc.

© 2016 Pearson Education, Inc.

© 2016 Pearson Education, Inc.

 In mammals, pathogen recognition triggers release

© 2016 Pearson Education, Inc.

 The inflammatory response, such as pain and

© 2016 Pearson Education, Inc.

© 2016 Pearson Education, Inc.

Red blood cells

© 2016 Pearson Education, Inc.

© 2016 Pearson Education, Inc.

 Adaptations have evolved in some pathogens that

© 2016 Pearson Education, Inc.

© 2016 Pearson Education, Inc.

Mature B cell Mature T cell

© 2016 Pearson Education, Inc.

© 2016 Pearson Education, Inc.

 Each B cell antigen receptor is a Y-shaped

© 2016 Pearson Education, Inc.

© 2016 Pearson Education, Inc.

© 2016 Pearson Education, Inc.

(b) Antigen receptor specificity

© 2016 Pearson Education, Inc.

(b) Antigen receptor specificity

© 2016 Pearson Education, Inc.

 Each T cell receptor consists of two different

© 2016 Pearson Education, Inc.

© 2016 Pearson Education, Inc.

© 2016 Pearson Education, Inc.

© 2016 Pearson Education, Inc.

 The adaptive immune system has four major

© 2016 Pearson Education, Inc.

 By combining variable elements, the immune

© 2016 Pearson Education, Inc.

© 2016 Pearson Education, Inc.

Recombination deletes DNA between

pre-mRNA V39 J5 Intron C

mRNA Cap V39 J5 C Poly-A tail