Chapter 43

Chapter 43
The Immune System
Overview: Reconnaissance, Recognition, and

Response
Barriers help an animal to defend itself from the
many dangerous pathogens it may encounter
The immune system recognizes foreign
bodies and responds with the production of
immune cells and proteins
PowerPoint Lecture Presentations for
Biology
Two major kinds of defense have evolved:

innate immunity and acquired immunity
Eighth Edition
Neil Campbell and Jane Reece
Lectures by Chris Romero, updated by Erin Barley with contributions from Joan Sharp
Copyright 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
Fig. 43-1
Innate immunity is present before any

exposure to pathogens and is effective from
the time of birth
It involves nonspecific responses to pathogens
Innate immunity consists of external barriers
plus internal cellular and chemical defenses
1.5 m
Fig. 43-2
Pathogens
(microorganisms
and viruses)
Acquired immunity, or adaptive immunity,

develops after exposure to agents such as
microbes, toxins, or other foreign substances
It involves a very specific response to
pathogens
INNATE IMMUNITY
Recognition of traits
shared by broad ranges
of pathogens, using a
small set of receptors
Rapid response
ACQUIRED IMMUNITY
Recognition of traits
specific to particular
pathogens, using a vast
array of receptors
Barrier defenses:
Skin
Mucous membranes
Secretions
Internal defenses:
Phagocytic cells
Antimicrobial proteins
Inflammatory response
Natural killer cells
Humoral response:
Antibodies defend against
infection in body fluids.
Cell-mediated response:
Cytotoxic lymphocytes defend
against infection in body cells.
Slower response
Concept 43.1: In innate immunity, recognition and

response rely on shared traits of pathogens
Innate Immunity of Invertebrates
Both invertebrates and vertebrates depend on

innate immunity to fight infection
In insects, an exoskeleton made of chitin forms

the first barrier to pathogens
Vertebrates also develop acquired immune

defenses
The digestive system is protected by low pH

and lysozyme, an enzyme that digests
microbial cell walls
Hemocytes circulate within hemolymph and
carry out phagocytosis, the ingestion and
digestion of foreign substances including
bacteria
Fig. 43-3
Microbes
Hemocytes also secrete antimicrobial peptides

that disrupt the plasma membranes of bacteria
PHAGOCYTIC CELL
Vacuole
Lysosome
containing
enzymes
Fig. 43-4
The immune system recognizes bacteria and

fungi by structures on their cell walls
An immune response varies with the class of
pathogen encountered
Fig. 43-5
Fig. 43-5a
RESULTS
RESULTS
Wild type
75
Mutant + drosomycin
100
50
25
0
0
24
48
72
96
Hours post-infection
120
Fruit fly survival after infection by N. crassa fungi
% survival
100
Wild type
75
Mutant +
defensin
Mutant +
drosomycin
75
Mutant + drosomycin
50
Mutant + defensin
Mutant
25
0
50
25
Wild type
Mutant + defensin
Mutant
%s
survival
% survival
100
Mutant
24
48
72
96
120
0
0
24
48
72
96
Fruit fly survival after infection by N. crassa fungi
120
Fruit fly survival after infection by M. luteus bacteria
Fig. 43-5b
Innate Immunity of Vertebrates
RESULTS
The immune system of mammals is the best

understood of the vertebrates
%s
survival
100
Wild type
75
Mutant +
defensin
Innate defenses include barrier defenses,

phagocytosis, antimicrobial peptides
50
Mutant +
drosomycin
25
M t t
Mutant
0
0
24
48
72
96
120
Additional defenses are unique to vertebrates:

the inflammatory response and natural killer
cells
Fruit fly survival after infection by M. luteus bacteria

Barrier Defenses
Cellular Innate Defenses
Barrier defenses include the skin and mucous

membranes of the respiratory, urinary, and
reproductive tracts
White blood cells (leukocytes) engulf

pathogens in the body
Mucus traps and allows for the removal of

microbes
Groups of pathogens are recognized by TLR,

Toll-like receptors
Many body fluids including saliva, mucus, and

tears are hostile to microbes
The low pH of skin and the digestive system
prevents growth of microbes
Fig. 43-6
EXTRACELLULAR
Lipopolysaccharide
FLUID
Helper
protein
TLR4
Flagellin
WHITE
BLOOD
CELL
A white blood cell engulfs a microbe, then

fuses with a lysosome to destroy the microbe
TLR5
There are different types of phagocytic cells:

Neutrophils engulf and destroy microbes
VESICLE
Macrophages are part of the lymphatic

system and are found throughout the body
TLR9
CpG DNA
TLR3
Inflammatory
responses
Eosinophils discharge destructive enzymes
ds RNA
Dendritic cells stimulate development of

acquired immunity
Fig. 43-7
Antimicrobial Peptides and Proteins
Interstitial fluid
Adenoid
Tonsil
Blood
capillary
Lymph
nodes
Spleen
Tissue
cells
Lymphatic
vessel
Peyers patches
(small intestine)
Appendix
Lymphatic
vessels
Peptides and proteins function in innate

defense by attacking microbes directly or
impeding their reproduction
Interferon proteins provide innate defense
against viruses and help activate macrophages
About 30 proteins make up the complement
system, which causes lysis of invading cells
and helps trigger inflammation
Lymph
node
Masses of
defensive cells
Inflammatory Responses
Following an injury, mast cells release
histamine, which promotes changes in blood
vessels; this is part of the inflammatory
response
These changes increase local blood supply
and allow more phagocytes and antimicrobial
proteins to enter tissues
Fig. 43-8-1
Pathogen
Splinter
Chemical Macrophage
i
l
signals
Mast cell
Capillary
Red blood cells Phagocytic cell
Pus, a fluid rich in white blood cells, dead

microbes, and cell debris, accumulates at the
site of inflammation
Fig. 43-8-2
Pathogen
Fig. 43-8-3
Splinter
Chemical Macrophage
i
l
signals
Mast cell
Pathogen
Fluid
Capillary
Splinter
Chemical Macrophage
i
l
signals
Mast cell
Capillary
Fluid
Phagocytosis
Natural Killer Cells

Inflammation can be either local or systemic
(throughout the body)
All cells in the body (except red blood cells)

have a class 1 MHC protein on their surface
Fever is a systemic inflammatory response

triggered by pyrogens released by
macrophages, and toxins from
f
pathogens
Cancerous or infected cells no longer express

this protein; natural killer (NK) cells attack
these damaged cells
Septic shock is a life-threatening condition

caused by an overwhelming inflammatory
response
Innate Immune System Evasion by Pathogens
Concept 43.2: In acquired immunity, lymphocyte

receptors provide pathogen-specific recognition
Some pathogens avoid destruction by

modifying their surface to prevent recognition
or by resisting breakdown following
phagocytosis
White blood cells called lymphocytes

recognize and respond to antigens, foreign
molecules
Tuberculosis (TB) is one such disease and kills

more than a million people a year
Lymphocytes that mature in the thymus above

the heart are called T cells, and those that
mature in bone marrow are called B cells
Acquired Immunity: An Overview

Lymphocytes contribute to immunological
memory, an enhanced response to a foreign
molecule encountered previously
Cytokines are secreted by macrophages and
dendritic cells to recruit and activate
lymphocytes
B cells and T cells have receptor proteins that

can bind to foreign molecules
Each individual lymphocyte is specialized to
recognize a specific type of molecule
Fig. 43-9
Antigen Recognition by Lymphocytes

An antigen is any foreign molecule to which a
lymphocyte responds
Antigenbinding
site
Antigenbinding site
Antigenbinding
site
Disulfide
bridge
A single B cell or T cell has about 100,000

identical antigen receptors
Light
chain
Variable
regions
Constant
regions
Transmembrane
region
Plasma
membrane
chain
Heavy chains
chain
Disulfide bridge
B cell
Cytoplasm of B cell
T cell
Cytoplasm of T cell
(a) B cell receptor
(b) T cell receptor
Fig. 43-9a
Fig. 43-9b
Antigenbinding site
Antigenbinding
site
Antigenbinding
site
Disulfide
bridge
Variable
regions
Variable
regions
Constant
regions
Constant
regions
Light
chain
Transmembrane
region
Plasma
membrane
Heavy chains
Transmembrane
region
Plasma
membrane
chain
chain
Disulfide bridge
B cell
(a) B cell receptor
Cytoplasm of B cell
Cytoplasm of T cell
T cell
(b) T cell receptor
Fig. 43-10
All antigen receptors on a single lymphocyte

recognize the same epitope, or antigenic
determinant, on an antigen
B cells give rise to plasma cells, which secrete
proteins called antibodies or
immunoglobulins
Antigenbinding
sites
Epitopes
(antigenic
determinants)
Antigen-binding sites
Antibody A Antigen Antibody C
C
Antibody B
The Antigen Receptors of B Cells and T Cells

B cell receptors bind to specific, intact
antigens
The B cell receptor consists of two identical
heavy chains and two identical light chains
Secreted antibodies, or immunoglobulins, are

structurally similar to B cell receptors but lack
transmembrane regions that anchor receptors
in the plasma membrane
The tips of the chains form a constant (C)

region, and each chain contains a variable (V)
region, so named because its amino acid
sequence varies extensively from one B cell to
another
Each T cell receptor consists of two different

polypeptide chains
T cells bind to antigen fragments presented on

a host cell
The tips of the chain form a variable (V) region;

the rest is a constant (C) region
These antigen fragments are bound to cellsurface proteins called MHC molecules
T cells can bind to an antigen that is free or on

the surface of a pathogen
MHC molecules are so named because they

are encoded by a family of genes called the
major histocompatibility complex
Video: T Cell Receptors

The Role of the MHC
Fig. 43-11
Top view: binding surface

exposed to antigen receptors
In infected cells, MHC molecules bind and

transport antigen fragments to the cell surface,
a process called antigen presentation
A nearby T cell can then detect the antigen
fragment displayed on the cells surface
Antigen
Class I MHC
molecule
Antigen
Depending on their source, peptide antigens

are handled by different classes of MHC
molecules
Plasma
membrane of
infected cell
Fig. 43-12
Infected cell
Microbe
Class I MHC molecules are found on almost

all nucleated cells of the body
They display peptide antigens to cytotoxic T
cells
Antigenpresenting
cell
1 Antigen
associates
with MHC
molecule
Antigen
fragment
Antigen
fragment
1
1
Class I MHC
molecule
T cell
receptor
(a)
Class II MHC
molecule
T cell
receptor
2 T cell
recognizes
combination
Cytotoxic T cell
(b)
Helper T cell
Lymphocyte Development
Class II MHC molecules are located mainly on
dendritic cells, macrophages, and B cells
Dendritic cells, macrophages, and B cells are
antigen-presenting cells that display antigens
to cytotoxic T cells and helper T cells
The acquired immune system has three

important properties:
Receptor diversity
A lack of reactivity against host cells
Immunological memory
Fig. 43-13
Generation of Lymphocyte Diversity by Gene

Rearrangement
DNA of undifferentiated B cell

V37
Differences in the variable region account for

specificity of antigen receptors
V38
V39
1 DNA deleted between randomly selected V and J

segments
V37
V38
V39 J5 Intron
Functional gene
2 Transcription
pre mRNA
pre-mRNA
V39 J5
Intron
3 RNA processing
V39 J5
mRNA Cap
B cell receptor
Poly-A tail
V
V
4 Translation
Rearranged DNA is transcribed and translated

and the antigen receptor formed
DNA of differentiated B cell
The immunoglobulin (Ig) gene encodes one

chain of the B cell receptor
Many different chains can be produced from
the same Ig chain gene by rearrangement of
the DNA
J1 J2 J3 J4 J5 Intron
V40
V
C
Light-chain polypeptide
Variable
region
C
Constant
region
B cell
Origin of Self-Tolerance
Amplifying Lymphocytes by Clonal Selection
Antigen receptors are generated by random

rearrangement of DNA
In the body there are few lymphocytes with

antigen receptors for any particular epitope
As lymphocytes mature in bone marrow or the

thymus, they are tested for self-reactivity
The binding of a mature lymphocyte to an

antigen induces the lymphocyte to divide
rapidly
Lymphocytes with receptors specific for the

bodys own molecules are destroyed by
apoptosis, or rendered nonfunctional
This proliferation of lymphocytes is called

clonal selection
Two types of clones are produced: short-lived
activated effector cells and long-lived
memory cells
Fig. 43-14
Antigen molecules
B cells that
differ in
antigen
specificity
Antigen
receptor
The first exposure to a specific antigen

represents the primary immune response
During this time, effector B cells called plasma
cells are generated, and T cells are activated
to their effector forms
In the secondary immune response, memory
cells facilitate a faster, more efficient response
Antibody
molecules
Clone of memory cells
Clone of plasma cells
Animation: Role of B Cells

Fig. 43-15
Antibody
y concentration
(arbitrary units)
Primary immune response

to antigen A produces
antibodies to A.
Secondary immune response to

antigen A produces antibodies to A;
primary immune response to antigen
B produces antibodies to B.
Acquired immunity has two branches: the

humoral immune response and the cellmediated immune response
104
103
Antibodies
to A
102
Humoral immune response involves

activation and clonal selection of B cells
cells,
resulting in production of secreted antibodies
Antibodies
to B
101
100
Concept 43.3: Acquired immunity defends against

infection of body cells and fluids
14
21
Exposure
to antigen A
28
35
42
49
56
Exposure to
antigens A and B
Cell-mediated immune response involves

activation and clonal selection of cytotoxic T
cells
Helper T cells aid both responses
Time (days)
Fig. 43-16
Fig. 43-16a
Humoral (antibody-mediated) immune response
Key
Antigen (1st exposure)
Engulfed by
Antigenpresenting cell
Humoral (antibody-mediated) immune response
Cell-mediated immune response
Stimulates
Gives rise to
Key
+

Stimulates
Gives rise to
Engulfed by
B cell
Helper T cell
Cytotoxic T cell
B cell
Helper T cell
M
Memory
Helper T cells
Memory
Helper T cells
Antigen (2nd exposure)

Plasma cells
Memory B cells
Memory
Cytotoxic T cells
Active
Cytotoxic T cells
Secreted
antibodies
Plasma cells
+
Memory
B cells
Secreted
antibodies
Defend against extracellular pathogens by binding to antigens,

thereby neutralizing pathogens or making them better targets
for phagocytes and complement proteins.
Fig. 43-16b
Defend against intracellular pathogens

and cancer by binding to and lysing the
infected cells or cancer cells.
Cell-mediated immune response

Key
+

Engulfed by
Helper T Cells: A Response to Nearly All Antigens
Stimulates
Gives rise to
A surface protein called CD4 binds the class II

MHC molecule
+
Helper T cell
Defend against extracellular pathogens
Cytotoxic T cell
Memory
Helper T cells
+
+
+
Active
Cytotoxic T cells
This binding keeps the helper T cell joined to

the antigen-presenting cell while activation
occurs
Activated helper T cells secrete cytokines that
stimulate other lymphocytes
Memory
Cytotoxic T cells
Animation: Helper T Cells
Defend against intracellular pathogens
10
Fig. 43-17
Cytotoxic T Cells: A Response to Infected Cells
Antigenpresenting
cell
Cytotoxic T cells are the effector cells in cellmediated immune response
Peptide antigen
Cytotoxic T cells make CD8, a surface protein

that greatly enhances interaction between a
target
g cell and a cytotoxic
y
T cell
Bacterium
Class II MHC molecule
CD4
TCR (T cell receptor)
Helper T cell
Cytokines
Humoral
immunity
(secretion of
antibodies by
plasma cells)
+
B cell
+
+
Cytotoxic T cell
Cell-mediated
immunity
(attack on
infected cells)
Binding to a class I MHC complex on an

infected cell activates a cytotoxic T cell and
makes it an active killer
The activated cytotoxic T cell secretes proteins
that destroy the infected target cell
Animation: Cytotoxic T Cells
Fig. 43-18-1
Fig. 43-18-2
Cytotoxic T cell
Cytotoxic T cell
Perforin
Perforin
Granzymes
CD8
Granzymes
CD8
TCR
Class I MHC
molecule
Target
cell
TCR
Class I MHC
molecule
Target
cell
Peptide
antigen
Fig. 43-18-3
Pore
Peptide
antigen
B Cells: A Response to Extracellular Pathogens
Released cytotoxic T cell
The humoral response is characterized by

secretion of antibodies by B cells
Cytotoxic T cell
Perforin
Granzymes
CD8
TCR
Class I MHC
molecule
Target
cell
y g target
g cell
Dying
Pore
Peptide
antigen
Activation of B cells is aided by cytokines and

antigen binding to helper T cells
Clonal selection of B cells generates antibodysecreting plasma cells, the effector cells of
humoral immunity
11
Fig. 43-19
Fig. 43-19-1
Bacterium
Antigen-presenting cell
Peptide B cell
antigen
Bacterium
Peptide
antigen
Class II MHC
molecule
TCR
CD4
Cytokines
Secreted
antibody
molecules
Class II MHC
molecule
TCR
Endoplasmic
reticulum
ti l
off
plasma cell
Helper T cell
Activated
helper T cell
CD4
Clone of memory
B cells
Helper T cell
2 m
Fig. 43-19-2
Fig. 43-19-3
Bacterium
Peptide
antigen
Class II MHC
molecule
TCR
B cell
Helper T cell
B cell
Class II MHC
molecule
+
CD4
Bacterium
Peptide
antigen
TCR
Cytokines
Activated
helper T cell
Helper T cell
Fig. 43-19a
+
CD4
Cytokines
Activated
helper T cell
Secreted
antibody
molecules
Clone of memory
B cells
Antibody Classes
Endoplasmic
reticulum of
plasma cell
The five major classes of antibodies, or

immunoglobulins, differ in distribution and
function
Polyclonal antibodies are the products of many
different
ff
clones off B cells following
f
exposure to
a microbial antigen
Monoclonal antibodies are prepared from a
single clone of B cells grown in culture
2 m
12
Fig. 43-20
Fig. 43-20a
Class of Immunoglobulin (Antibody)
IgM
(pentamer)
Distribution
Function
First Ig class
produced after
initial exposure to
antigen; then its
concentration in
the blood declines
Promotes neutralization and crosslinking of antigens;

very effective in
complement system
activation
Most abundant Ig
class in blood;
also present in
tissue fluids
Promotes opsonization, neutralization,

and cross-linking of
antigens; less effective in activation of
complement system
than IgM
J chain
IgG
(monomer)

IgM
(pentamer)
Only Ig class that

crosses placenta,
thus conferring
passive immunity
on fetus
IgA
g
(dimer)
J chain
Present in
secretions such
as tears, saliva,
mucus, and
breast milk
Provides localized
defense of mucous
membranes by
cross-linking and
neutralization of
antigens
Presence in breast
milk confers
passive immunity
on nursing infant
Secretory
component
IgE
(monomer)
Present in blood
at low concentrations
Triggers release from

mast cells and
basophils of histamine and other
chemicals that cause
allergic reactions
IgD
(monomer)
Present primarily
on surface of
B cells that have
not been exposed
to antigens
Acts as antigen
receptor in the
antigen-stimulated
proliferation and
differentiation of
B cells (clonal
selection)
Transmembrane
region
Distribution
First Ig class
produced after
initial exposure to
antigen;
ti
then
th its
it
concentration in
the blood declines
Function
Promotes neutralization and crosslinking of antigens;

very effective
ff ti in
i
complement system
activation
J chain
Fig. 43-20b
Fig. 43-20c

IgG
(monomer)
Distribution
Most abundant Ig
class in blood;
also present in
tissue fluids
Function
Promotes opsonization, neutralization,

and cross-linking of
antigens; less effective in activation of
complement system
than IgM
Only Ig class that
crosses placenta,
thus conferring
passive immunity
on fetus
Fig. 43-20d
IgA
(dimer)
J chain
Distribution
Present in
secretions such
as tears, saliva,
mucus, and
b
breast
t milk
ilk
Function
Provides localized
defense of mucous
membranes by
cross-linking and
neutralization
li i
off
antigens
Presence in breast
milk confers
passive immunity
on nursing infant
Secretory
component
Fig. 43-20e

IgE
((monomer)
o o e)
Distribution
Present in blood
at low concentrations
Function
Triggers release from
mast cells and
basophils of histamine and other
chemicals that cause
allergic reactions

IgD
(monomer)
Transmembrane
region
Distribution
Present primarily
on surface of
B cells that have
not been exposed
to antigens
Function
Acts as antigen
receptor in the
antigen-stimulated
proliferation and
differentiation of
B cells (clonal
selection)
13
Fig. 43-21
The Role of Antibodies in Immunity

Neutralization occurs when a pathogen can no
longer infect a host because it is bound to an
antibody
Viral neutralization
Opsonization
Activation of complement system and pore formation
Bacterium
Complement proteins
Virus
Formation of
membrane
attack complex
Opsonization occurs when antibodies bound to

antigens increase phagocytosis
Flow of water
and ions
Macrophage
Pore
Antibodies together with proteins of the

complement system generate a membrane
attack complex and cell lysis
Foreign
cell
Animation: Antibodies
Fig. 43-21a
Fig. 43-21b
Opsonization
Viral neutralization
Bacterium
Virus
Macrophage
Fig. 43-21c
Active and Passive Immunization
Activation of complement system and pore formation
Active immunity develops naturally in

response to an infection
Complement proteins
Formation of
membrane
attack complex
o of
o water
ate
Flow
and ions
Pore
It can also develop following immunization,

also called vaccination
In immunization, a nonpathogenic form of a
microbe or part of a microbe elicits an immune
response to an immunological memory
Foreign
cell
14
Fig. 43-22
Passive immunity provides immediate, shortterm protection

It is conferred naturally when IgG crosses the
placenta from mother to fetus or when IgA
passes from mother to infant in breast milk
It can be conferred artificially by injecting
antibodies into a nonimmune person
Immune Rejection
Blood Groups
Cells transferred from one person to another

can be attacked by immune defenses
Antigens on red blood cells determine whether

a person has blood type A (A antigen), B (B
antigen), AB (both A and B antigens), or O
(neither antigen)
This complicates blood transfusions or the

transplant of tissues or organs
Antibodies to nonself blood types exist in the

body
Transfusion with incompatible blood leads to
destruction of the transfused cells
Recipient-donor combinations can be fatal or
safe
Tissue and Organ Transplants

MHC molecules are different among genetically
nonidentical individuals
Differences in MHC molecules stimulate
rejection of tissue grafts and organ transplants
Chances of successful transplantation increase

if donor and recipient MHC tissue types are
well matched
Immunosuppressive drugs facilitate
transplantation
Lymphocytes in bone marrow transplants may
cause the donor tissue to reject the recipient
15
Concept 43.4: Disruption in immune system

function can elicit or exacerbate disease
Exaggerated, Self-Directed, and Diminished

Immune Responses
Some pathogens have evolved to diminish the

effectiveness of host immune responses
If the delicate balance of the immune system is

disrupted, effects range from minor to often
fatal
Allergies
Allergies are exaggerated (hypersensitive)
responses to antigens called allergens
Fig. 43-23
IgE
Histamine
Allergen
In localized allergies such as hay fever, IgE

antibodies produced after first exposure to an
allergen attach to receptors on mast cells
Granule
Mast cell
Autoimmune Diseases
The next time the allergen enters the body, it
binds to mast cellassociated IgE molecules
Mast cells release histamine and other
mediators that cause vascular changes leading
to typical allergy symptoms
An acute allergic response can lead to
anaphylactic shock, a life-threatening reaction
that can occur within seconds of allergen
exposure
In individuals with autoimmune diseases, the

immune system loses tolerance for self and
turns against certain molecules of the body
Autoimmune diseases include systemic lupus
erythematosus, rheumatoid arthritis, insulindependent diabetes mellitus, and multiple
sclerosis
16
Fig. 43-24
Exertion, Stress, and the Immune System

Moderate exercise improves immune system
function
Psychological stress has been shown to disrupt
hormonal, nervous, and immune systems
Immunodeficiency Diseases
Acquired Immune System Evasion by Pathogens
Inborn immunodeficiency results from

hereditary or developmental defects that
prevent proper functioning of innate, humoral,
and/or cell-mediated defenses
Pathogens have evolved mechanisms to attack

immune responses
Acquired immunodeficiency results from

exposure to chemical and biological agents
Acquired immunodeficiency syndrome
(AIDS) is caused by a virus
Antigenic Variation
Fig. 43-25
The human influenza virus mutates rapidly, and

new flu vaccines must be made each year
Human viruses occasionally exchange genes
with the viruses of domesticated animals
This poses a danger as human immune
systems are unable to recognize the new viral
strain
Million
ns of parasites
per mL of blood
1.5
Through antigenic variation, some pathogens

are able to change epitope expression and
prevent recognition
Antibodies to
variant 1
appear
Antibodies to Antibodies to
variant 3
variant 2
appear
appear
1.0
Variant 1
Variant 2
Variant 3
0.5
0
25
26
27
Weeks after infection
28
17
Latency
Attack on the Immune System: HIV
Some viruses may remain in a host in an

inactive state called latency
Human immunodeficiency virus (HIV) infects

helper T cells
Herpes simplex viruses can be present in a

human host without causing symptoms
The loss of helper T cells impairs both the

humoral and cell-mediated immune responses
and leads to AIDS
HIV eludes the immune system because of
antigenic variation and an ability to remain
latent while integrated into host DNA
Animation: HIV Reproductive Cycle
Fig. 43-26
AIDS
Helper T cell concentration

in blood (cells/mm3)
Latency
Relative antibody
concentration
800
People with AIDS are highly susceptible to

opportunistic infections and cancers that take
advantage of an immune system in collapse
Relative HIV
concentration
600
The spread of HIV is a worldwide problem
Helper T cell
concentration
400
The best approach for slowing this spread is

education about practices that transmit the
virus
200
0
0
2
3
4
5
6
7
8
Years after untreated infection
10
Cancer and Immunity
Fig. 43-UN1
Stem cell
Cell division and gene rearrangement
The frequency of certain cancers increases

when the immune response is impaired
Elimination of
self-reactive
B cells
Antigen
Two suggested explanations are

Immune system normally suppresses
cancerous cells
Clonal selection
Formation of activated cell populations
Increased inflammation increases the risk of

cancer
Antibody
Memory cells
Effector B cells
Microbe
Receptors bind to antigens
18
Fig. 43-UN2
You should now be able to:

1. Distinguish between innate and acquired
immunity
2. Name and describe four types of phagocytic
cells
3. Describe the inflammation response
4. Distinguish between the following pairs of

terms: antigens and antibodies; antigen and
epitope; B lymphocytes and T lymphocytes;
antibodies and B cell receptors; primary and
secondary immune responses; humoral and
cell-mediated
ll
di t d response; active
ti and
d passive
i
immunity
5. Explain how B lymphocytes and T
lymphocytes recognize specific antigens
6. Explain why the antigen receptors of
lymphocytes are tested for self-reactivity
7. Describe clonal selection and distinguish

between effector cells and memory cells
8. Describe the cellular basis for immunological
memory
9. Explain how a single antigen can provoke a
robust humoral response
10. Compare the processes of neutralization and
opsonization
11. Describe the role of MHC in the rejection of

tissue transplants
12. Describe an allergic reaction, including the
roles of IgE, mast cells, and histamine
13. Describe some of the mechanisms that
pathogens have evolved to thwart the
immune response of their hosts
14. List strategies that can reduce the risk of HIV
transmission
19

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Chapter 43

The Immune System

Overview: Reconnaissance, Recognition, and

PowerPoint Lecture Presentations for

Two major kinds of defense have evolved:

Copyright 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings

Innate immunity is present before any

Acquired immunity, or adaptive immunity,

Copyright 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings

Concept 43.1: In innate immunity, recognition and

Innate Immunity of Invertebrates

Both invertebrates and vertebrates depend on

In insects, an exoskeleton made of chitin forms

Vertebrates also develop acquired immune

The digestive system is protected by low pH

Copyright 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings

Copyright 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings

Hemocytes also secrete antimicrobial peptides

Copyright 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings

The immune system recognizes bacteria and

Copyright 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings

Fruit fly survival after infection by N. crassa fungi

Fruit fly survival after infection by N. crassa fungi

Fruit fly survival after infection by M. luteus bacteria

Innate Immunity of Vertebrates

The immune system of mammals is the best

Innate defenses include barrier defenses,

Additional defenses are unique to vertebrates:

Fruit fly survival after infection by M. luteus bacteria

Cellular Innate Defenses

Barrier defenses include the skin and mucous

White blood cells (leukocytes) engulf

Mucus traps and allows for the removal of

Groups of pathogens are recognized by TLR,

Many body fluids including saliva, mucus, and

Copyright 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings

A white blood cell engulfs a microbe, then

There are different types of phagocytic cells:

Macrophages are part of the lymphatic

Eosinophils discharge destructive enzymes

Dendritic cells stimulate development of

Antimicrobial Peptides and Proteins

Peptides and proteins function in innate

Red blood cells Phagocytic cell

Pus, a fluid rich in white blood cells, dead

Red blood cells Phagocytic cell

Red blood cells Phagocytic cell

Natural Killer Cells

All cells in the body (except red blood cells)

Fever is a systemic inflammatory response

Cancerous or infected cells no longer express

Septic shock is a life-threatening condition

Copyright 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings

Copyright 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings

Innate Immune System Evasion by Pathogens

Concept 43.2: In acquired immunity, lymphocyte

Some pathogens avoid destruction by

White blood cells called lymphocytes

Tuberculosis (TB) is one such disease and kills

Lymphocytes that mature in the thymus above

Copyright 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings

Copyright 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings

Acquired Immunity: An Overview

Copyright 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings