Download Chapt24ImmunSyst

Immune System
Chapter 24
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
An AIDS Uproar
• Acquired immune deficiency syndrome (AIDS)
– Is epidemic throughout much of the world
• Thousands of people are infected every day
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
• HIV, the virus that causes AIDS, attacks the
immune system
– And eventually destroys the body’s ability
to fight infection
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
INNATE DEFENSES AGAINST INFECTION
24.1 Innate defenses against infection include
the skin and mucous membranes, phagocytic
cells, and antimicrobial proteins
• Innate immunity
– Is present and effective long before exposure
to pathogens
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
• Microbes that breach the body’s external
defenses
– Are engulfed and destroyed by
macrophages
Bacteria
Figure 24.1A
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
• Interferons are proteins produced by virusinfected cells
–
That help other cells resist viruses
Viral nucleic acid
Antiviral proteins block
viral reproduction
1
2
Interferon
genes
turned
on
New viruses
DNA
mRNA
3
5
Interferon
molecules
Interferon stimulates
cell to turn on genes
for antiviral proteins
4
Figure 24.1B
Host cell 1
Makes interferon;
is killed by virus
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
Host cell 2
Protected against virus
by interferon from cell 1
24.2 The inflammatory response mobilizes
nonspecific defense forces
• Tissue damage triggers the inflammatory response
Pin
Skin surface
Swelling
Bacteria
Phagocytes and
fluid move
into area
Chemical
signals
Phagocytes
White
blood cell
Blood vessel
1 Tissue injury; release of chemical signals
such as histamine
2 Dilation and increased leakiness of local
blood vessels; migration of phagocytes
to the area
Figure 24.2
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
3
Phagocytes (macrophages and
neutrophils) consume bacteria and cell
debris; tissue heals
• The inflammatory response
– Can disinfect tissues and limit further
infection
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
24.3 The lymphatic system becomes a crucial
battleground during infection
• The lymphatic system
–
Is a network of lymphatic vessels and organs
Adenoid
Tonsil
Lymph nodes
Right lymphatic
duct, entering
vein
Thoracic duct,
entering vein
Lymph node
Masses of
lymphocytes and
macrophages
Thymus
Valve
Thoracic
duct
Lymphatic vessel
Blood capillary
Tissue cells
Appendix
Bone
marrow
Figure 24.3
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
Spleen
Interstitial fluid
Lymphatic
vessels
Lymphatic
capillary
• The vessels collect fluid from body tissues
– And return it as lymph to the blood
• Lymph organs such as the spleen and lymph
nodes
– Are packed with white blood cells that
fight infections
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
ACQUIRED IMMUNITY
24.4 The immune response counters specific
invaders
• Our immune system
– Responds to foreign molecules called
antigens
• The immune system reacts to antigens
– And “remembers” an invader
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
• We can temporarily acquire passive immunity
– By receiving “premade” antibodies
• Infection or vaccination
– Triggers active immunity
Figure 24.4
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
24.5 Lymphocytes mount a dual defense
• Two kinds of lymphocytes carry out the immune response
– B cells secrete antibodies that attack antigens
–
T cells attack cells infected with pathogens
Bone marrow
Thymus
Stem cell
Via
blood
Immature lymphocyte
Antigen
receptors
T cell
Cell-mediated
immunity
B cell
Humoral
immunity
Via
blood
Lymph nodes, spleen, and
other lymphatic organs
Other parts of the
lymphatic system
Figure 24.5A
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
Final maturation of
B and T cells in
lymphatic organ
• Millions of kinds of B cells and T cells, each
with different membrane receptors
– Wait in the lymphatic system, where they
may respond to invaders
Figure 24.5B
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
24.6 Antigens have specific regions where
antibodies bind to them
• Antigenic determinants
– Are the specific regions on an antigen to
which antibodies bind
Antibody A
molecules
Antigenbinding sites
Antigenic
determinants
Antigen
molecule
Antibody B
molecule
Figure 24.6
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
24.7 Clonal selection musters defensive forces
against specific antigens
• When an antigen enters the body
–
It activates only a small subset of
lymphocytes with complementary
receptors
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
• The selected lymphocyte cells multiply into
clones of short-lived effector cells
– Specialized for defending against the
antigen that triggered the response
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
The Steps of Clonal Selection
• In the primary immune response, clonal
selection
– Produces effector cells and memory cells
that may confer lifelong immunity
• In the secondary immune response
– Memory cells are activated by a second
exposure to the same antigen, which
initiates a faster and more massive
response
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
• The primary and secondary immune responses
Primary immune
response
2
1
Antigen
molecules
Antigen receptor
(antibody on cell
surface)
B cells with different
response
3 First exposure
antigen
Cell activation:
growth, division,
and differentiation
Antibody
molecules
4
5
5
Endoplasmic
reticulum
Clone of memory cells
Plasma (effector) cells secreting antibodies
Antigen
molecules
6 Second exposure
to same antigen
Secondary immune Antibody
molecules
response
Figure 24.7A
Endoplasmic
reticulum
Plasma (effector) cells secreting antibodies
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
Clone of memory cells
Primary vs. Secondary Immune Response
•
The primary immune response
–
Is slower than the secondary immune response
Antibody concentration
Second exposure
to antigen X, first
exposure to antigen
Y
First exposure to
antigen X
Primary immune
response to
antigen X
Primary immune
response to
antigen Y
Antibodies
to Y
Antibodies
to X
Figure 24.7B
Secondary immune
response to antigen
X
0
7
14
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
21
28
Time (days)
35
42
49
56
24.8 Antibodies are the weapons of humoral
immunity
• Antibody molecules
–
Are secreted by plasma (effector) B cells
Figure 24.8A
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
• An antibody molecule
– Has antigen-binding sites specific to the
antigenic determinants that elicited its
secretion
Antigen-binding
sites
Light
chain
C
Figure 24.8B
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
C
Heavy
chain
24.9 Antibodies mark antigens for elimination
• Antibodies promote antigen elimination
– Through several mechanisms
Binding of antibodies to antigens
inactivates antigens by
Neutralization
(blocks viral binding
sites; coats bacteria)
Agglutination
of microbes
Activation of
Complement system
Complement
molecule
Bacteria
Virus
Antigen
molecules
Bacterium
Figure 24.9
Precipitation of
dissolved antigens
Foreign cell
Enhances
Leads to
Phagocytosis
Cell Iysis
Macrophage
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
Hole
CONNECTION
24.10 Monoclonal antibodies are powerful tools in the
lab and clinic
• Monoclonal antibodies
–
Are produced by fusing B cells specific for a single
antigenic determinant with easy to grow tumor cells
Antigen injected
into mouse
B cells (from
spleen)
Tumor cells grown
in culture
Tumor cells
Cells fused to
generate hybrid
cells
Single hybrid cell
grown in culture
Antibody
Figure 24.10A
Hybrid cell culture,
producing monoclonal antibodies
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
• These molecules
– Are useful in research, diagnosis, and
treatment of certain cancers
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
24.11 Helper T cells stimulate humoral and cellmediated immunity
• Helper T cells and cytotoxic T cells
–
Are the main effectors of cell-mediated
immunity
• Helper T cells
–
Also stimulate the humoral responses
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
• In cell-mediated immunity, an antigenpresenting cell
– Displays a foreign antigen and one of the
body’s own self proteins to a helper T cell
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
• The helper T cell’s receptors
– Recognize the self-nonself complexes
and the interaction activates the helper
T cells
• The helper T cell
– Can then activate cytotoxic T cells and
B cells
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
• The activation of a helper T cell and its roles in
immunity
Self-nonself
complex
Microbe
B cell
T cell
receptor
Interleukin-2
stimulates
cell division
Macrophage
5
3
1
Humoral
Immunity
(secretion of
antibodies by
plasma cells)
6
Helper
T cell
2
7
4
Interleukin-2
activates
other B cells
and T cells
Self protein
Antigen from microbe
(nonself molecule)
Antigen-presenting
cell
Interleukin-1
stimulates
helper T cell
Figure 24.11
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
Binding
site for
antigen
Binding
site for self
protein
Cytotoxic
T cell
Cell-mediated
immunity
(attack on
infected cells)
CONNECTION
24.12 HIV destroys helper T cells, compromising the
body’s defenses
• The AIDS virus attacks helper T Cells
–
Opening the way for opportunistic infection
Figure 24.12
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
24.13 Cytotoxic T cells destroy infected body cells
• Cytotoxic T cells
–
Bind to infected body cells and destroy them
2 Perforin makes holes in
infected cell’s membrane
and enzyme enters
1 Cytotoxic T cell binds
to infected cell
Self-nonself
complex
Hole
forming
Foreign
antigen
Infecte cell
Perforin
molecule
Cytotoxic
T cell
Enzyme that
can promote
apoptosis
Figure 24.13
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
3 Infected cell
is destroyed
24.14 Cytotoxic T cells may help prevent cancer
• Cytotoxic T cells may attack cancer cells
– Which have abnormal surface molecules
Figure 24.14
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
24.15 The immune system depends on our
molecular fingerprints
• The immune system
– Normally reacts only against nonself
substances, not against self
– May reject transplanted organs because
these cells lack the unique “fingerprint” of
the recipient’s self proteins
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
DISORDERS OF THE IMMUNE SYSTEM
CONNECTION
24.16 Malfunction or failure of the immune system causes
disease
• In autoimmune diseases
–
The system turns against the body’s own molecules
• In immunodeficiency diseases
–
Immune components are lacking, and frequent
infections recur
• Physical and emotional stress
–
May weaken the immune system
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
CONNECTION
24.17 Allergies are overreactions to certain
environmental antigens
• Allergies
– Are abnormal sensitivities to antigens
(allergens) in the surroundings
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
• The two stages of an allergic reaction
B cell
(plasma cell)
Mast
cell
Antigenic determinant
Histamine
1
Allergen (pollen grain)
enters blood stream
2
B cells make
antibodies
3
Antibodies
attach to
mast cell
4
Sensitization: Initial exposure to allergen
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
5
Histamine is
released, causing
allergy symptoms
Later exposure to same allergen
3
Figure 24.17
Allergen binds to
antibodies on
mast cell
Antibodies
attach to
mast cell