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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 © 2008 Pearson Education, Inc., publishing as Pearson Benjamin 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
• 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
• Slower response
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.
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
% survival
100
Wild type
75
Mutant + drosomycin
50
Mutant + defensin
Mutant
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
50
Mutant +
drosomycin
25
Mutant
0
0
24
48
72
96
Hours post-infection
Fruit fly survival after infection by M. luteus bacteria
120
Fig. 43-5a
RESULTS
% survival
100
Wild type
75
Mutant + drosomycin
50
Mutant
25
Mutant + defensin
0
0
24
48
72
96
Hours post-infection
Fruit fly survival after infection by N. crassa fungi
120
Fig. 43-5b
RESULTS
% survival
100
Wild type
75
Mutant +
defensin
50
Mutant +
drosomycin
25
Mutant
0
0
24
48
72
96
Hours post-infection
120
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
Lipopolysaccharide
FLUID
Helper
protein
TLR4
WHITE
BLOOD
CELL
Flagellin
TLR5
VESICLE
CpG DNA
TLR9
TLR3
ds RNA
Inflammatory
responses
• 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
capillary
Lymph
nodes
Spleen
Tissue
cells
Lymphatic
vessel
Peyer’s patches
(small intestine)
Appendix
Lymphatic
vessels
Lymph
node
Masses of
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
Chemical Macrophage
signals
Mast cell
Capillary
Red blood cells Phagocytic cell
Fig. 43-8-2
Pathogen
Splinter
Chemical Macrophage
signals
Mast cell
Capillary
Red blood cells Phagocytic cell
Fluid
Fig. 43-8-3
Pathogen
Splinter
Chemical Macrophage
signals
Mast cell
Capillary
Red blood cells Phagocytic cell
Fluid
Phagocytosis
• 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
Antigenbinding
site
Antigenbinding site
Antigenbinding
site
Disulfide
bridge
C
C
Light
chain
Variable
regions
V
V
Constant
regions
C
C
Transmembrane
region
Plasma
membrane
Heavy chains
 chain
 chain
Disulfide bridge
B cell
(a) B cell receptor
Cytoplasm of B cell
Cytoplasm of T cell
(b) T cell receptor
T cell
Fig. 43-9a
Antigenbinding site
Antigenbinding
site
Disulfide
bridge
Variable
regions
C
C
Constant
regions
Light
chain
Transmembrane
region
Plasma
membrane
Heavy chains
B cell
(a) B cell receptor
Cytoplasm of B cell
Fig. 43-9b
Antigenbinding
site
Variable
regions
V
V
Constant
regions
C
C
Transmembrane
region
Plasma
membrane
 chain
 chain
Disulfide bridge
Cytoplasm of T cell
(b) T cell receptor
T cell
• 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
Antigenbinding
sites
Antigen-binding sites
Antibody A Antigen Antibody C
C
C
Antibody B
Epitopes
(antigenic
determinants)
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
Video: T Cell Receptors
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• T cells bind to antigen fragments presented on
a host cell
• These antigen fragments are bound to cellsurface 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 MHC
molecule
Antigen
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
Antigenpresenting
cell
1 Antigen
associates
with MHC
molecule
Antigen
fragment
Antigen
fragment
1
Class I MHC
molecule
1
T cell
receptor
(a)
2
2
Cytotoxic T cell
Class II MHC
molecule
T cell
receptor
2 T cell
recognizes
combination
(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
V39 J5
mRNA Cap
C
B cell receptor
Poly-A tail
V
V
V
4 Translation
V
C
C
Light-chain polypeptide
V
Variable
region
C
C
Constant
region
B cell
C
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
Animation: Role of B Cells
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Fig. 43-15
Antibody 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.
104
103
Antibodies
to A
102
Antibodies
to B
101
100
0
7
Exposure
to antigen A
14
21
28
35
42
Exposure to
antigens A and B
Time (days)
49
56
Concept 43.3: Acquired immunity defends against
infection of body cells and fluids
• Acquired immunity has two branches: the
humoral immune response and the cellmediated 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 response
Cell-mediated immune response
Key
Antigen (1st exposure)
+
Engulfed by
Gives rise to
Antigenpresenting cell
+
Stimulates
+
+
B cell
Helper T cell
+
Cytotoxic T cell
+
Memory
Helper T cells
+
+
+
Antigen (2nd exposure)
Plasma cells
Memory B cells
+
Memory
Cytotoxic T cells
Active
Cytotoxic T cells
Secreted
antibodies
Defend against extracellular pathogens by binding to antigens,
thereby neutralizing pathogens or making them better targets
for phagocytes and complement proteins.
Defend against intracellular pathogens
and cancer by binding to and lysing the
infected cells or cancer cells.
Fig. 43-16a
Humoral (antibody-mediated) immune response
Key
+
Antigen (1st exposure)
Stimulates
Gives rise to
Engulfed by
Antigenpresenting cell
+
+
B cell
Helper T cell
+
Memory
Helper T cells
+
Plasma cells
+
Antigen (2nd exposure)
Memory
B cells
Secreted
antibodies
Defend against extracellular pathogens
+
Fig. 43-16b
Cell-mediated immune response
Key
+
Antigen (1st exposure)
Engulfed by
Antigenpresenting cell
Stimulates
Gives rise to
+
+
Helper T cell
Cytotoxic T 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
Animation: Helper T Cells
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Fig. 43-17
Antigenpresenting
cell
Peptide antigen
Bacterium
Class II MHC molecule
CD4
TCR (T cell receptor)
Helper T cell
Humoral
immunity
(secretion of
antibodies by
plasma cells)
Cytokines
+
B cell
+
+
+
Cytotoxic T cell
Cell-mediated
immunity
(attack on
infected cells)
Cytotoxic T Cells: A Response to Infected Cells
• Cytotoxic T cells are the effector cells in cellmediated 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
Animation: Cytotoxic T Cells
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Fig. 43-18-1
Cytotoxic T cell
Perforin
Granzymes
CD8
TCR
Class I MHC
molecule
Target
cell
Peptide
antigen
Fig. 43-18-2
Cytotoxic T cell
Perforin
Granzymes
CD8
TCR
Class I MHC
molecule
Target
cell
Pore
Peptide
antigen
Fig. 43-18-3
Released cytotoxic T cell
Cytotoxic T cell
Perforin
Granzymes
CD8
TCR
Class I MHC
molecule
Target
cell
Dying target cell
Pore
Peptide
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 antibodysecreting plasma cells, the effector cells of
humoral immunity
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Fig. 43-19
Antigen-presenting cell
Bacterium
Peptide
antigen
B cell
Class II MHC
molecule
TCR
Clone of plasma cells
+
CD4
Cytokines
Secreted
antibody
molecules
Endoplasmic
reticulum of
plasma cell
Helper T cell
Activated
helper T cell
Clone of memory
B cells
2 µm
Fig. 43-19-1
Antigen-presenting cell
Bacterium
Peptide
antigen
Class II MHC
molecule
TCR
CD4
Helper T cell
Fig. 43-19-2
Antigen-presenting cell
Bacterium
Peptide
antigen
B cell
Class II MHC
molecule
TCR
+
CD4
Helper T cell
Cytokines
Activated
helper T cell
Fig. 43-19-3
Antigen-presenting cell
Bacterium
Peptide
antigen
B cell
Class II MHC
molecule
TCR
Clone of plasma cells
+
CD4
Helper T cell
Cytokines
Activated
helper T cell
Clone of memory
B cells
Secreted
antibody
molecules
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 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)
Only Ig class that
crosses placenta,
thus conferring
passive immunity
on fetus
IgA
(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
Fig. 43-20a
Class of Immunoglobulin (Antibody)
IgM
(pentamer)
J chain
Distribution
First Ig class
produced after
initial exposure to
antigen; then its
concentration in
the blood declines
Function
Promotes neutralization and crosslinking of antigens;
very effective in
complement system
activation
Fig. 43-20b
Class of Immunoglobulin (Antibody)
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. 43-20c
Class of Immunoglobulin (Antibody)
IgA
(dimer)
J chain
Secretory
component
Distribution
Present in
secretions such
as tears, saliva,
mucus, and
breast milk
Function
Provides localized
defense of mucous
membranes by
cross-linking and
neutralization of
antigens
Presence in breast
milk confers
passive immunity
on nursing infant
Fig. 43-20d
Class of Immunoglobulin (Antibody)
IgE
(monomer)
Distribution
Present in blood
at low concentrations
Function
Triggers release from
mast cells and
basophils of histamine and other
chemicals that cause
allergic reactions
Fig. 43-20e
Class of Immunoglobulin (Antibody)
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)
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
Animation: Antibodies
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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
and ions
Macrophage
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, 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
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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, insulindependent 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
Millions of parasites
per mL of blood
1.5
Antibodies to
variant 1
appear
Antibodies to Antibodies to
variant 2
variant 3
appear
appear
1.0
Variant 1
Variant 2
Variant 3
0.5
0
25
26
27
Weeks after infection
28
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
Animation: HIV Reproductive Cycle
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Fig. 43-26
AIDS
Helper T cell concentration
in blood (cells/mm3)
Latency
Relative antibody
concentration
800
Relative HIV
concentration
600
Helper T cell
concentration
400
200
0
0
1
2
3
4
5
6
7
8
Years after untreated infection
9
10
• 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
Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
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
Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
Chapter 45
Hormones and the
Endocrine 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 © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
Overview: The Body’s Long-Distance Regulators
• Animal hormones are chemical signals that
are secreted into the circulatory system and
communicate regulatory messages within the
body
• Hormones reach all parts of the body, but only
target cells are equipped to respond
• Insect metamorphosis is regulated by
hormones
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• Two systems coordinate communication
throughout the body: the endocrine system and
the nervous system
• The endocrine system secretes hormones
that coordinate slower but longer-acting
responses including reproduction,
development, energy metabolism, growth, and
behavior
• The nervous system conveys high-speed
electrical signals along specialized cells called
neurons; these signals regulate other cells
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Fig. 45-1
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Fig. 45-UN1
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Concept 45.1: Hormones and other signaling
molecules bind to target receptors, triggering
specific response pathways
• Chemical signals bind to receptor proteins on
target cells
• Only target cells respond to the signal
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Types of Secreted Signaling Molecules
• Secreted chemical signals include
– Hormones
– Local regulators
– Neurotransmitters
– Neurohormones
– Pheromones
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Hormones
• Endocrine signals (hormones) are secreted into
extracellular fluids and travel via the
bloodstream
• Endocrine glands are ductless and secrete
hormones directly into surrounding fluid
• Hormones mediate responses to environmental
stimuli and regulate growth, development, and
reproduction
Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
Fig. 45-2
Blood
vessel
Response
(a) Endocrine signaling
Response
(b) Paracrine signaling
Response
(c) Autocrine signaling
Synapse
Neuron
Response
(d) Synaptic signaling
Neurosecretory
cell
Blood
vessel
(e) Neuroendocrine signaling
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Response
• Exocrine glands have ducts and secrete
substances onto body surfaces or into body
cavities (for example, tear ducts)
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Local Regulators
• Local regulators are chemical signals that
travel over short distances by diffusion
• Local regulators help regulate blood pressure,
nervous system function, and reproduction
• Local regulators are divided into two types
– Paracrine signals act on cells near the
secreting cell
– Autocrine signals act on the secreting cell
itself
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Fig. 45-2a
Blood
vessel
Response
(a) Endocrine signaling
Response
(b) Paracrine signaling
Response
(c) Autocrine signaling
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Neurotransmitters and Neurohormones
• Neurons (nerve cells) contact target cells at
synapses
• At synapses, neurons often secrete chemical
signals called neurotransmitters that diffuse a
short distance to bind to receptors on the target
cell
• Neurotransmitters play a role in sensation,
memory, cognition, and movement
Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
Fig. 45-2b
Synapse
Neuron
Response
(d) Synaptic signaling
Neurosecretory
cell
Blood
vessel
(e) Neuroendocrine signaling
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Response
• Neurohormones are a class of hormones that
originate from neurons in the brain and diffuse
through the bloodstream
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Pheromones
• Pheromones are chemical signals that are
released from the body and used to
communicate with other individuals in the
species
• Pheromones mark trails to food sources, warn
of predators, and attract potential mates
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Chemical Classes of Hormones
• Three major classes of molecules function as
hormones in vertebrates:
– Polypeptides (proteins and peptides)
– Amines derived from amino acids
– Steroid hormones
Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
• Lipid-soluble hormones (steroid hormones)
pass easily through cell membranes, while
water-soluble hormones (polypeptides and
amines) do not
• The solubility of a hormone correlates with the
location of receptors inside or on the surface of
target cells
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Fig. 45-3
Water-soluble
Lipid-soluble
0.8 nm
Polypeptide:
Insulin
Steroid:
Cortisol
Amine:
Epinephrine
Amine:
Thyroxine
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Hormone Receptor Location: Scientific Inquiry
• In the 1960s, researchers studied the
accumulation of radioactive steroid hormones in
rat tissue
• These hormones accumulated only in target cells
that were responsive to the hormones
• These experiments led to the hypothesis that
receptors for the steroid hormones are located
inside the target cells
• Further studies have confirmed that receptors for
lipid-soluble hormones such as steroids are
located inside cells
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• Researchers hypothesized that receptors for
water-soluble hormones would be located on
the cell surface
• They injected a water-soluble hormone into the
tissues of frogs
• The hormone triggered a response only when it
was allowed to bind to cell surface receptors
• This confirmed that water-soluble receptors
were on the cell surface
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Fig. 45-4
RESULTS
MSH injected into melanocyte
Melanocyte
with melanosomes
(black dots)
Melanosomes
do not disperse
Melanosomes
disperse
Nucleus
MSH injected into interstitial fluid (blue)
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Cellular Response Pathways
• Water and lipid soluble hormones differ in their
paths through a body
• Water-soluble hormones are secreted by
exocytosis, travel freely in the bloodstream,
and bind to cell-surface receptors
• Lipid-soluble hormones diffuse across cell
membranes, travel in the bloodstream bound to
transport proteins, and diffuse through the
membrane of target cells
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• Signaling by any of these hormones involves
three key events:
– Reception
– Signal transduction
– Response
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Fig. 45-5-1
Fat-soluble
hormone
Watersoluble
hormone
Signal receptor
Transport
protein
TARGET
CELL
(a)
Signal
receptor
NUCLEUS
(b)
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Fig. 45-5-2
Fat-soluble
hormone
Watersoluble
hormone
Transport
protein
Signal receptor
TARGET
CELL
Cytoplasmic
response
OR
Signal
receptor
Gene
regulation
Cytoplasmic
response
(a)
NUCLEUS
(b)
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Gene
regulation
Pathway for Water-Soluble Hormones
• Binding of a hormone to its receptor initiates a
signal transduction pathway leading to
responses in the cytoplasm, enzyme activation,
or a change in gene expression
Animation: Water-Soluble Hormone
Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
• The hormone epinephrine has multiple effects
in mediating the body’s response to short-term
stress
• Epinephrine binds to receptors on the plasma
membrane of liver cells
• This triggers the release of messenger
molecules that activate enzymes and result in
the release of glucose into the bloodstream
Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
Fig. 45-6-1
Epinephrine
Adenylyl
cyclase
G protein
G protein-coupled
receptor
GTP
ATP
cAMP
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Second
messenger
Fig. 45-6-2
Epinephrine
Adenylyl
cyclase
G protein
G protein-coupled
receptor
GTP
ATP
cAMP
Inhibition of
glycogen synthesis
Protein
kinase A
Promotion of
glycogen breakdown
Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
Second
messenger
Pathway for Lipid-Soluble Hormones
• The response to a lipid-soluble hormone is
usually a change in gene expression
• Steroids, thyroid hormones, and the hormonal
form of vitamin D enter target cells and bind to
protein receptors in the cytoplasm or nucleus
• Protein-receptor complexes then act as
transcription factors in the nucleus, regulating
transcription of specific genes
Animation: Lipid-Soluble Hormone
Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
Fig. 45-7-1
Hormone
(estradiol)
Estradiol
(estrogen)
receptor
Plasma
membrane
Hormone-receptor
complex
Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
Fig. 45-7-2
Hormone
(estradiol)
Estradiol
(estrogen)
receptor
Plasma
membrane
Hormone-receptor
complex
DNA
Vitellogenin
mRNA
for vitellogenin
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Multiple Effects of Hormones
• The same hormone may have different effects
on target cells that have
– Different receptors for the hormone
– Different signal transduction pathways
– Different proteins for carrying out the response
• A hormone can also have different effects in
different species
Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
Fig. 45-8-1
Same receptors but different
intracellular proteins (not shown)
Epinephrine
Epinephrine
 receptor
 receptor
Glycogen
deposits
Glycogen
breaks down
and glucose
is released.
(a) Liver cell
Vessel
dilates.
(b) Skeletal muscle
blood vessel
Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
Fig. 45-8-2
Same receptors but different
intracellular proteins (not shown)
Different receptors
Epinephrine
Epinephrine
Epinephrine
 receptor
 receptor
 receptor
Glycogen
deposits
Glycogen
breaks down
and glucose
is released.
(a) Liver cell
Vessel
dilates.
(b) Skeletal muscle
blood vessel
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Vessel
constricts.
(c) Intestinal blood
vessel
Fig. 45-9
(a)
(b)
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Fig. 45-9a
(a)
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Fig. 45-9b
(b)
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Signaling by Local Regulators
• In paracrine signaling, nonhormonal chemical
signals called local regulators elicit responses
in nearby target cells
• Types of local regulators:
– Cytokines and growth factors
– Nitric oxide (NO)
– Prostaglandins
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• Prostaglandins help regulate aggregation of
platelets, an early step in formation of blood
clots
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Concept 45.2: Negative feedback and antagonistic
hormone pairs are common features of the
endocrine system
• Hormones are assembled into regulatory
pathways
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Fig. 45-10
Major endocrine glands:
Hypothalamus
Pineal gland
Pituitary gland
Thyroid gland
Parathyroid glands
Organs containing
endocrine cells:
Thymus
Heart
Adrenal
glands
Testes
Liver
Stomach
Pancreas
Kidney
Kidney
Small
intestine
Ovaries
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Simple Hormone Pathways
• Hormones are released from an endocrine cell,
travel through the bloodstream, and interact
with the receptor or a target cell to cause a
physiological response
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Fig. 45-11
Pathway
–
Example
Stimulus
Low pH in
duodenum
S cells of duodenum
secrete secretin ( )
Endocrine
cell
Blood
vessel
Target
cells
Response
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Pancreas
Bicarbonate release
• A negative feedback loop inhibits a response
by reducing the initial stimulus
• Negative feedback regulates many hormonal
pathways involved in homeostasis
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Insulin and Glucagon: Control of Blood Glucose
• Insulin and glucagon are antagonistic
hormones that help maintain glucose
homeostasis
• The pancreas has clusters of endocrine cells
called islets of Langerhans with alpha cells
that produce glucagon and beta cells that
produce insulin
Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
Fig. 45-12-1
Insulin
Beta cells of
pancreas
release insulin
into the blood.
STIMULUS:
Blood glucose level
rises.
Homeostasis:
Blood glucose level
(about 90 mg/100 mL)
Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
Fig. 45-12-2
Body cells
take up more
glucose.
Insulin
Beta cells of
pancreas
release insulin
into the blood.
Liver takes
up glucose
and stores it
as glycogen.
STIMULUS:
Blood glucose level
rises.
Blood glucose
level declines.
Homeostasis:
Blood glucose level
(about 90 mg/100 mL)
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Fig. 45-12-3
Homeostasis:
Blood glucose level
(about 90 mg/100 mL)
STIMULUS:
Blood glucose level
falls.
Alpha cells of pancreas
release glucagon.
Glucagon
Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
Fig. 45-12-4
Homeostasis:
Blood glucose level
(about 90 mg/100 mL)
STIMULUS:
Blood glucose level
falls.
Blood glucose
level rises.
Alpha cells of pancreas
release glucagon.
Liver breaks
down glycogen
and releases
glucose.
Glucagon
Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
Fig. 45-12-5
Body cells
take up more
glucose.
Insulin
Beta cells of
pancreas
release insulin
into the blood.
Liver takes
up glucose
and stores it
as glycogen.
STIMULUS:
Blood glucose level
rises.
Blood glucose
level declines.
Homeostasis:
Blood glucose level
(about 90 mg/100 mL)
STIMULUS:
Blood glucose level
falls.
Blood glucose
level rises.
Alpha cells of pancreas
release glucagon.
Liver breaks
down glycogen
and releases
glucose.
Glucagon
Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
Target Tissues for Insulin and Glucagon
• Insulin reduces blood glucose levels by
– Promoting the cellular uptake of glucose
– Slowing glycogen breakdown in the liver
– Promoting fat storage
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• Glucagon increases blood glucose levels by
– Stimulating conversion of glycogen to glucose
in the liver
– Stimulating breakdown of fat and protein into
glucose
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Diabetes Mellitus
• Diabetes mellitus is perhaps the best-known
endocrine disorder
• It is caused by a deficiency of insulin or a
decreased response to insulin in target tissues
• It is marked by elevated blood glucose levels
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• Type I diabetes mellitus (insulin-dependent) is
an autoimmune disorder in which the immune
system destroys pancreatic beta cells
• Type II diabetes mellitus (non-insulindependent) involves insulin deficiency or
reduced response of target cells due to change
in insulin receptors
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