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Chapter 43

The Immune System

PowerPoint ® Lecture
Presentations for

Biology
Eighth Edition
Neil Campbell and Jane Reece
Lectures by Chris Romero, updated by Erin Barley with contributions from Joan Sharp
Copyright
Copyright©©2008
2008Pearson
PearsonEducation,
Education,Inc.,
Inc.,publishing
publishingasasPearson
PearsonBenjamin
BenjaminCummings
Cummings
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
• Two major kinds of defense have evolved:
innate immunity and acquired immunity

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Fig. 43-1

1.5 µm
• 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

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• 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

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Fig. 43-2

Pathogens
(microorganisms
and viruses)

INNATE IMMUNITY Barrier defenses:


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

ACQUIRED IMMUNITY Humoral response:


Antibodies defend against
• Recognition of traits infection in body fluids.
specific to particular
pathogens, using a vast Cell-mediated response:
array of receptors 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
• Both invertebrates and vertebrates depend on
innate immunity to fight infection
• Vertebrates also develop acquired immune
defenses

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Innate Immunity of Invertebrates

• In insects, an exoskeleton made of chitin forms


the first barrier to pathogens
• 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

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Fig. 43-3

Microbes

PHAGOCYTIC CELL

Vacuole
Lysosome
containing
enzymes
• Hemocytes also secrete antimicrobial peptides
that disrupt the plasma membranes of
bacteria

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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

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Fig. 43-5
RESULTS

100 Wild type

75

% survival
Mutant + drosomycin
50
Mutant Mutant + defensin
25

0
0 24 48 72 96 12
0
Hours post-infection
Fruit fly survival after infection by N. crassa fungi

100

75 Wild type Mutant +


% survival

defensin
50
Mutant + Mutant
25 drosomycin

0
0 24 48 72 96 12
0
Hours post-infection
Fruit fly survival after infection by M. luteus bacteria
Fig. 43-5a

RESULTS

1 Wild type
0
0
7
% survival

5 Mutant + drosomycin
5
0
Mutant Mutant + defensin
2
5
0
0 24 48 72 96 1
Hours post-infection 2
0
Fruit fly survival after infection by N. crassa fungi
Fig. 43-5b

RESULTS

100

75 Wild type Mutant +


% survival

defensin
50
Mutant + Mutant
25 drosomycin

0
0 24 48 72 96 120
Hours post-infection
Fruit fly survival after infection by M. luteus bacteria
Innate Immunity of Vertebrates

• The immune system of mammals is the best


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

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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 microbes
• The low pH of skin and the digestive system
prevents growth of microbes

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Cellular Innate Defenses

• White blood cells (leukocytes) engulf


pathogens in the body
• Groups of pathogens are recognized by TLR,
Toll-like receptors

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Fig. 43-6

EXTRACELLULAR
FLUID Lipopolysaccharide
Helper
protein Flagellin
TLR4
WHITE
BLOOD
CELL
TLR5

VESICLE
TLR9
CpG
DNA
TLR3 Inflammatory
responses

ds RNA
• A white blood cell engulfs a microbe, then
fuses with a lysosome to destroy the microbe
• There are different types of phagocytic cells:
– Neutrophils engulf and destroy microbes
– Macrophages are part of the lymphatic
system and are found throughout the
body
– Eosinophils discharge destructive
enzymes
– Dendritic cells stimulate development of
acquired immunity
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Fig. 43-7
Interstitial fluid
Adenoid

Tonsil

Blood
Lymph capillary
nodes

Spleen Tissue Lymphatic


cells vessel
Peyer’s patches
(small intestine)
Appendi
x

Lymphatic
vessels Lymph Masses of
node defensive cells
Antimicrobial Peptides and Proteins

• 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

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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
• Pus, a fluid rich in white blood cells, dead
microbes, and cell debris, accumulates at the
site of inflammation

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Fig. 43-8-1

Pathogen Splinter

Chemica Macrophag
l e
Mast signals
cel
l Capillary

Red blood Phagocytic cell


cells
Fig. 43-8-2

Pathogen Splinter

Chemica Macrophag
l e Fluid
Mast signals
cel
l Capillary

Red blood Phagocytic cell


cells
Fig. 43-8-3

Pathogen Splinter

Chemica Macrophag
l e Fluid
Mast signals
cel
l Capillary Phagocytosis

Red blood Phagocytic cell


cells
• Inflammation can be either local or systemic
(throughout the body)
• Fever is a systemic inflammatory response
triggered by pyrogens released by
macrophages, and toxins from pathogens
• Septic shock is a life-threatening condition
caused by an overwhelming inflammatory
response

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Natural Killer Cells

• All cells in the body (except red blood cells)


have a class 1 MHC protein on their surface
• Cancerous or infected cells no longer express
this protein; natural killer (NK) cells attack
these damaged cells

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Innate Immune System Evasion by Pathogens

• Some pathogens avoid destruction by


modifying their surface to prevent recognition
or by resisting breakdown following
phagocytosis
• Tuberculosis (TB) is one such disease and kills
more than a million people a year

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Concept 43.2: In acquired immunity, lymphocyte
receptors provide pathogen-specific recognition
• White blood cells called lymphocytes
recognize and respond to antigens, foreign
molecules
• Lymphocytes that mature in the thymus above
the heart are called T cells, and those that
mature in bone marrow are called B cells

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• 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

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Acquired Immunity: An Overview

• 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

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Antigen Recognition by Lymphocytes

• An antigen is any foreign molecule to which a


lymphocyte responds
• A single B cell or T cell has about 100,000
identical antigen receptors

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Fig. 43-9

Antigen- Antigen- Antigen-


binding binding site binding
site site

Disulfid

V
e
V
bridge

V
Variable
regions V V

C
C

C C Constant C C
regions
Light
chain
Transmembrane
region

Plasma
membrane
Heavy  chain  chain
chain Disulfide bridge
s
B cell Cytoplasm of B Cytoplasm of T cell T cell
cell
(a) B cell receptor (b) T cell receptor
Fig. 43-9a

Antigen- Antigen-
binding binding site
site

Disulfide

V
bridge

V
Variable
regions

C
C
Constant
C C
regions
Light
chain
Transmembran
e
region

Plasma
membrane
Heavy chains

B cell Cytoplasm of B cell

(a) B cell receptor


Fig. 43-9b
Antigen-
binding
site

Variable
regions V V
Constant C C
regions

Transmembrane
region

Plasma
membrane
 chain  chain
Disulfide bridge
Cytoplasm of T cell T cell

(b) T cell receptor


• 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

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Fig. 43-10

Antigen-
binding Epitopes
sites (antigenic
determinants)
Antigen-binding
sites

Antibody A Antigen Antibody C


V

V
V

V
C
C

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
• 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

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• Secreted antibodies, or immunoglobulins, are
structurally similar to B cell receptors but lack
transmembrane regions that anchor
receptors in the plasma membrane

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• Each T cell receptor consists of two different
polypeptide chains
• The tips of the chain form a variable (V) region;
the rest is a constant (C) region
• T cells can bind to an antigen that is free or on
the surface of a pathogen

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• T cells bind to antigen fragments presented on
a host cell
• These antigen fragments are bound to cell-
surface proteins called MHC molecules
• MHC molecules are so named because they
are encoded by a family of genes called the
major histocompatibility complex

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The Role of the MHC

• 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 cell’s surface
• Depending on their source, peptide antigens
are handled by different classes of MHC
molecules

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Fig. 43-11

Top view: binding surface


exposed to antigen receptors

Antigen
Class I Antigen
MHC
molecule

Plasma
membrane of
infected cell
• Class I MHC molecules are found on almost
all nucleated cells of the body
• They display peptide antigens to cytotoxic T
cells

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Fig. 43-12

Infected cell Microbe Antigen-


presenting
1 Antigen cell
associates
with MHC
molecule
Antigen
fragment Antigen
fragment
1
1
Class I MHC Class II MHC
molecule 2 molecule
2
T cell T cell
2 T cell receptor
receptor
recognizes
combination

(a) Cytotoxic T cell (b) Helper T cell


• 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

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Lymphocyte Development

• The acquired immune system has three


important properties:
– Receptor diversity
– A lack of reactivity against host cells
– Immunological memory

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Generation of Lymphocyte Diversity by Gene
Rearrangement
• Differences in the variable region account for
specificity of antigen receptors
• 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
• Rearranged DNA is transcribed and translated
and the antigen receptor formed

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Fig. 43-13
DNA of undifferentiated B cell
V37 V38 V39 V40 J1 J2 J3 J4 J5 Intron C

1 DNA deleted between randomly selected V and J


segments
DNA of differentiated B cell
V37 V38 V39 J5 Intron C

Functional gene

2 Transcription

pre-mRNA V39 J5 Intron C

3 RNA processing

B cell receptor
mRNA Ca V39 J5 C Poly-A tail
p
V V
V V
4 Translation
C C

C C
Light-chain polypeptide V C

Variable Consta
region nt B cell
region
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
• Lymphocytes with receptors specific for the
body’s own molecules are destroyed by
apoptosis, or rendered nonfunctional

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Amplifying Lymphocytes by Clonal Selection

• In the body there are few lymphocytes with


antigen receptors for any particular epitope
• The binding of a mature lymphocyte to an
antigen induces the lymphocyte to divide
rapidly
• This proliferation of lymphocytes is called
clonal selection
• Two types of clones are produced: short-lived
activated effector cells and long-lived
memory cells

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Fig. 43-14
Antigen molecules

B cells that
differ in
antigen
specificity Antigen
receptor

Antibody
molecules

Clone of memory cells Clone of plasma cells


• 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

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Fig. 43-15
Primary immune response Secondary immune response to
to antigen A produces antigen A produces antibodies to A;
antibodies to A. primary immune response to
antigen
B produces antibodies to 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 43.3: Acquired immunity defends against
infection of body cells and fluids
• Acquired immunity has two branches: the
humoral immune response and the cell-
mediated immune response
• Humoral immune response involves
activation and clonal selection of B cells,
resulting in production of secreted antibodies
• Cell-mediated immune response involves
activation and clonal selection of cytotoxic T
cells
• Helper T cells aid both responses

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Fig. 43-16
Humoral (antibody-mediated) immune Cell-mediated immune response
response
Key
Antigen (1st
exposure) + Stimulates
Engulfed by Gives rise
to

Antigen-
+ presenting cell +

B cell + Helper T cell Cytotoxic T cell


+

Memory
Helper T cells

+ + +

Antigen (2nd
exposure)
+ Memory Active
Plasma cells Memory B Cytotoxic T Cytotoxic T
cells cells cells

Secreted
antibodies

Defend against extracellular pathogens by binding to antigens, Defend against intracellular pathogens
thereby neutralizing pathogens or making them better targets and cancer by binding to and lysing
for phagocytes and complement proteins. the
infected cells or cancer cells.
Fig. 43-16a
Humoral (antibody-mediated) immune response
Key Antigen (1st
+ Stimulates exposure)
Engulfed by
Gives rise to
Antigen-
+ presenting cell

B cell Helper T
+ cell

Memory
Helper T cells

+ +
Antigen (2nd
Memory exposure)
Plasma cells +
B cells

Secreted
antibodies

Defend against extracellular


pathogens
Fig. 43-16b
Cell-mediated immune
response
Antigen (1st Key
exposure) + Stimulates
Engulfed by
Gives rise to
Antigen-
presenting cell
+

Helper T Cytotoxic T cell


cell +

Memory
Helper T cells

+ +
Antigen (2nd
exposure) Active
+ Cytotoxic T cells

Memory
Cytotoxic T cells

Defend against intracellular pathogens


Helper T Cells: A Response to Nearly All Antigens

• A surface protein called CD4 binds the class II


MHC molecule
• 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

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Fig. 43-17

Antigen-
presenting Peptide antigen
cell
Bacterium

Class II MHC molecule


CD4
TCR (T cell receptor)
Helper T
cell
Cytokines +
Humoral +
immunity Cell-
(secretion of mediate
+ + d
antibodies by
plasma cells) B cell immunity
Cytotoxic T cell
(attack on
infected
cells)
Cytotoxic T Cells: A Response to Infected Cells

• Cytotoxic T cells are the effector cells in cell-


mediated immune response
• Cytotoxic T cells make CD8, a surface protein
that greatly enhances interaction between a
target cell and a cytotoxic T cell
• 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

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Fig. 43-18-1

Cytotoxic T cell

Perforin
Granzymes

CD8 TCR
Class I
MHC
molecule

Target Peptide
cell antigen
Fig. 43-18-2

Cytotoxic T cell

Perforin
Granzymes

CD8 TCR
Class I Pore
MHC
molecule

Target Peptide
cell antigen
Fig. 43-18-3

Released cytotoxic T cell


Cytotoxic T cell

Perforin
Granzymes

CD8 TCR Dying target cell


Class I Pore
MHC
molecule

Target Peptide
cell antigen
B Cells: A Response to Extracellular Pathogens

• The humoral response is characterized by


secretion of antibodies by B cells
• Activation of B cells is aided by cytokines and
antigen binding to helper T cells
• Clonal selection of B cells generates antibody-
secreting plasma cells, the effector cells of
humoral immunity

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Fig. 43-19

Antigen-presenting cell Bacterium

Peptide B cell
antigen

Class II MHC
molecule + Clone of plasma cells Secreted
antibody
TCR CD4 Cytokines molecules
Endoplasmic
reticulum of
plasma cell
Activated
Helper T cell helper T cell Clone of memory
B cells

2 µm
Fig. 43-19-1

Antigen-presenting cell Bacterium

Peptide
antigen

Class II
MHC
molecule
TC CD4
R

Helper T
cell
Fig. 43-19-2

Antigen-presenting cell Bacterium

Peptide B
antigen c
e
l
l
Class II
MHC +
molecule
TC CD4 Cytokines
R

Activated
Helper T helper T cell
cell
Fig. 43-19-3

Antigen-presenting cell Bacterium

Peptide B
antigen c
e
l
l
Class II
MHC + Clone of plasma Secreted
molecule cells antibody
TC CD4 Cytokines molecules
R

Activated
Helper T helper T cell Clone of memory
cell B cells
Fig. 43-19a

Endoplasmic
reticulum of
plasma cell

2 µm
Antibody Classes

• The five major classes of antibodies, or


immunoglobulins, differ in distribution and
function
• Polyclonal antibodies are the products of many
different clones of B cells following exposure
to a microbial antigen
• Monoclonal antibodies are prepared from a
single clone of B cells grown in culture

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Fig. 43-20
Class of Immuno-
globulin (Antibody) Distribution Function

IgM First Ig class Promotes


(pentamer) produced after neutraliz
initial exposure to a-
antigen; then its tion and cross-
concentration in linking of antigens;
the blood declines very effective in
complement system
J chain activation

IgG Most abundant Ig Promotes opsoniza-


(monomer class in blood; tion, neutralization,
) also present in and cross-linking of
tissue fluids antigens; less effec-
tive in activation of
complement system
than IgM

Only Ig class that


crosses placenta,
thus conferring
passive immunity
on fetus

IgA Present in Provides localized


(dimer) secretions such defense of mucous
as tears, saliva, membranes by
mucus, and cross-linking and
breast milk neutralization of
J chain antigens

Presence in breast
milk confers
Secretory passive immunity
component on nursing infant

IgE Present in blood Triggers release from


(monomer at low concen- mast cells and
) trations basophils of hista-
mine and other
chemicals that cause
allergic reactions

IgD Present primarily Acts as antigen


(monomer on surface of receptor in the
) B cells that have antigen-stimulated
not been exposed proliferation and
to antigens differentiation of
B cells (clonal
Trans- selection)
membrane
region
Fig. 43-20a

Class of Immuno-
Distribution Function
globulin (Antibody)

IgM First Ig class Promotes neutraliza-


(pentamer) produced after tion and cross-
initial exposure to linking of antigens;
antigen; then its very effective in
concentration in complement system
the blood declines activation
J chain
Fig. 43-20b

Class of Immuno-
Distribution Function
globulin (Antibody)

IgG Most abundant Ig Promotes opsoniza-


(monomer) class in blood; tion, neutralization,
also present in and cross-linking of
tissue fluids antigens; less effec-
tive in activation of
complement system
than IgM

Only Ig class that


crosses placenta,
thus conferring
passive immunity
on fetus
Fig. 43-20c

Class of Immuno-
Distribution Function
globulin (Antibody)

IgA Present in Provides localized


(dimer) secretions such defense of mucous
as tears, saliva, membranes by
mucus, and cross-linking and
J chain breast milk neutralization of
antigens

Presence in breast
milk confers
Secretory passive immunity
component on nursing infant
Fig. 43-20d

Class of Immuno-
Distribution Function
globulin (Antibody)

IgE Present in blood Triggers release from


(monomer) at low concen- mast cells and
trations basophils of hista-
mine and other
chemicals that cause
allergic reactions
Fig. 43-20e

Class of Immuno-
Distribution Function
globulin (Antibody)

IgD Present primarily Acts as antigen


(monomer) on surface of receptor in the
B cells that have antigen-stimulated
not been exposed proliferation and
to antigens differentiation of
B cells (clonal
Trans- selection)
membrane
region
The Role of Antibodies in Immunity

• Neutralization occurs when a pathogen can no


longer infect a host because it is bound to an
antibody
• Opsonization occurs when antibodies bound to
antigens increase phagocytosis
• Antibodies together with proteins of the
complement system generate a membrane
attack complex and cell lysis

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Fig. 43-21

Viral neutralization Opsonization Activation of complement system and pore formation


Bacterium
Complement proteins
Virus
Formation of
membrane
attack complex

Flow of water
Macrophage and ions

Pore

Foreign
cell
Fig. 43-21a

Viral neutralization

Virus
Fig. 43-21b

Opsonization
Bacterium

Macrophage
Fig. 43-21c

Activation of complement system and pore formation

Complement proteins

Formation of
membrane
attack complex

Flow of water
and ions

Pore

Foreign
cell
Active and Passive Immunization

• Active immunity develops naturally in


response to an infection
• 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

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• Passive immunity provides immediate, short-
term 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

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Fig. 43-22
Immune Rejection

• Cells transferred from one person to another


can be attacked by immune defenses
• This complicates blood transfusions or the
transplant of tissues or organs

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Blood Groups

• 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)
• 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

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Tissue and Organ Transplants

• MHC molecules are different among genetically


nonidentical individuals
• Differences in MHC molecules stimulate
rejection of tissue grafts and organ
transplants

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• 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

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Concept 43.4: Disruption in immune system
function can elicit or exacerbate disease
• Some pathogens have evolved to diminish the
effectiveness of host immune responses

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Exaggerated, Self-Directed, and Diminished
Immune Responses
• If the delicate balance of the immune system is
disrupted, effects range from minor to often
fatal

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Allergies

• Allergies are exaggerated (hypersensitive)


responses to antigens called allergens
• In localized allergies such as hay fever, IgE
antibodies produced after first exposure to an
allergen attach to receptors on mast cells

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Fig. 43-23

IgE
Histamine
Allergen

Granule
Mast cell
• The next time the allergen enters the body, it
binds to mast cell–associated 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

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Autoimmune Diseases

• 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, insulin-
dependent diabetes mellitus, and multiple
sclerosis

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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

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Immunodeficiency Diseases

• Inborn immunodeficiency results from


hereditary or developmental defects that
prevent proper functioning of innate,
humoral, and/or cell-mediated defenses
• Acquired immunodeficiency results from
exposure to chemical and biological agents
• Acquired immunodeficiency syndrome
(AIDS) is caused by a virus

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Acquired Immune System Evasion by Pathogens

• Pathogens have evolved mechanisms to attack


immune responses

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Antigenic Variation

• Through antigenic variation, some pathogens


are able to change epitope expression and
prevent recognition
• 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

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Fig. 43-25

1.5 Antibodies to Antibodies to Antibodies to


variant 1 variant 2 variant 3
appear appear appear
Millions of parasites
per mL of blood

1.0
Variant 1 Variant 2 Variant 3

0.5

0
25 26 27 28
Weeks after infection
Latency

• Some viruses may remain in a host in an


inactive state called latency
• Herpes simplex viruses can be present in a
human host without causing symptoms

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Attack on the Immune System: HIV

• Human immunodeficiency virus (HIV) infects


helper T cells
• 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

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Fig. 43-26

Latency AIDS

Relative antibody
concentration
800
Helper T cell concentration
in blood (cells/mm3)

Relative HIV
600 concentration
Helper T cell
concentration
400

200

0
0 1 2 3 4 5 6 7 8 9 10
Years after untreated infection
• People with AIDS are highly susceptible to
opportunistic infections and cancers that take
advantage of an immune system in collapse
• The spread of HIV is a worldwide problem
• The best approach for slowing this spread is
education about practices that transmit the
virus

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Cancer and Immunity

• The frequency of certain cancers increases


when the immune response is impaired
• Two suggested explanations are
– Immune system normally suppresses
cancerous cells
– Increased inflammation increases the risk of
cancer

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Fig. 43-UN1
Stem cell

Cell division and gene rearrangement

Elimination of
self-reactive
B cells
Antigen

Clonal selection

Formation of activated cell populations


Antibody

Memory cells Effector B cells

Microbe

Receptors bind to antigens


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

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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 response; active and passive
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

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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

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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

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