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Chapter 17
Functional
Anatomy of
Prokaryotic and
Eukaryotic Cells
© 2013 Pearson Education, Inc.
Lectures prepared by Christine L. Case
© 2013 Pearson Education, Inc.
Immunity
 Innate immunity: generic defenses against any
pathogen;
 should be born with this; instant protection
 Adaptive immunity: induced resistance to a
specific pathogen;
 occurs when you come into contact with a pathogen.
Specific
 Is achieved by Lymphocytes
 T-Cells
 B-Cells- Humoral immunity
 Immunity brought about by antibody
production
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Figure 17.20 The dual nature of the adaptive immune system.
Humoral (antibody-mediated) immune system
Cellular (cell-mediated) immune system
Control of freely circulating pathogens
Control of intracellular pathogens
Intracellular antigens are
expressed on the surface of an
APC, a cell infected by a virus, a
bacterium, or a parasite.
Extracellular antigens
A B cell binds to the
antigen for which it is
specific. A T-dependent B
cell requires cooperation
with a T helper (TH) cell.
T cell
Cytokines activate T
helper (TH) cell.
Cytokines activate
macrophage.
Cytokines
Cytokines
B cell
The B cell, often with
stimulation by cytokines
from a TH cell, differentiates
into a plasma cell. Some B
cells become memory cells.
Cytokines from the TH
cell transform B cells
into antibody-producing
plasma cells.
Plasma cells
proliferate and
produce antibodies
against the antigen.
Activation of
macrophage
(enhanced
phagocytic activity).
TH cell
Cytotoxic T
lymphocyte
Plasma cell
Memory cell
Some T and B cells differentiate
into memory cells that respond
rapidly to any secondary
encounter with an antigen.
Lysed target cell
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A T cell binds to
MHC–antigen
complexes on the
surface of the
infected cell,
activating the T cell
(with its cytokine
receptors).
The CD8+T cell
becomes a cytotoxic
T lymphocyte (CTL)
able to induce
apoptosis of the
target cell.
Dual Nature of Adaptive Immunity
 Humoral immunity
 Due to antibodies
 B cells- are responsible
for producing antibodies
 B cells mature in the bone
marrow
 Plasma cells- activated
B cells that actually
produce the antibodies.
 Memory Cells – activate
on subsequent
exposures.
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 Cellular immunity
 Due to T cells
 T cells- are responsible
for producing cytokines
which will send
instructions to other cells
(like B cells).
 T cells mature in the
thymus
 Are activated by macrophages
that have engulfed a bacteria and
presented its antigen on its cell
membrane
Figure 17.8 Differentiation of T cells and B cells.
Stem cells develop in bone
marrow or in fetal liver
Stem cell
(diverges into
two cell lines)
Red bone marrow
of adults
Thymus
Differentiate to B cells in
adult red bone marrow
Differentiate to
T cells in thymus
B cell
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T cell
Migrate to lymphoid
tissue such as spleen,
but especially lymph
nodes
Dual Nature of Adaptive Immunity
 Antigens (Ag)- Cell markers, non self antigens are
considered to be foreign and stimulate an immune
response.
 Antibodies(Ab)- produced by our bodies in
response to a foreign antigen
 Globular proteins called immunoglobulins
 When the antibody and antigen combine, clumping
occurs.
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Figure 17.3c The structure of a typical antibody molecule.
Antibodies
Antibody molecules shown by atomic
force microscopy (see page 64)
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IgG Antibodies
 80% of serum antibodies
 Triggers complement
system
 In blood, lymph, and
intestine
 Cross placenta (passive
immunity)
 Enhance phagocytosis;
neutralize toxins and
viruses; protect fetus and
newborn
 Half-life = 23 days indicates
there has been a immune
response
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IgM Antibodies
 5–10% of serum
antibodies
 Mainly stays In blood
 Responds to blood
group antigens
 Agglutinate microbes;
first Ab produced in
response to infection
 Half-life = 5 days
(better det. Of current
infection
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IgA Antibodies
 10–15% of serum
antibodies
 Most abundant in
secretions
 Mucosal protection
 Half-life = 6 days
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IgD Antibodies
 0.2% of serum
antibodies
 In blood, in lymph, and
on B cells
 On B cells, initiate
immune response
 No well know function
 Half-life = 3 days
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IgE Antibodies
 0.002% of serum
antibodies
 On mast cells, on
basophils, and in blood
 Respond to Allergic
reactions and of
parasitic worms
 Half-life = 2 days
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Activation of B Cells
 B cells differentiate into:
 Antibody-producing plasma cells
 Memory cells
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Antigen–Antibody Binding




Agglutination
Opsonization – coating with antibodies
Activation of complement –(IgG or IgM)
Antibody-dependent cell-mediated cytotoxicity
 Destruction is achieved by other cells besides antibody
secreting cells
 Neutralization – prevents attachment to other host
cells
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Figure 17.7 The results of antigen–antibody binding.
Agglutination
(see also Figure 18.5)
Reduces number of infectious
units to be dealt with
PROCTECTIVE
of complement
MECHANISM OF BINDING Activation
(see also Figure 16.9)
ANTIBODIES
Causes inflammation and
TO ANTIGENS
cell lysis
Complement
Bacteria
Bacterium
Lysis
Antibody-dependent
cell-mediated cytotoxicity
Opsonization
(see also Figure 16.9)
(see also Figure 17.16)
Antibodies attached to target cell cause
destruction by macrophages, eosinophils,
and NK cells
Coating antigen with antibody
enhances phagocytosis
Phagocyte
Eosinophil
Epitopes
Neutralization
Large target cell (parasite)
(see also Figure 18.9)
Blocks adhesion of
bacteria and
viruses to mucosa
Virus
Bacterium
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Toxin
Blocks
attachment of
toxin
Perforin and
lytic enzymes
T Cells and Cellular Immunity
 T cells mature in the thymus
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Table 17.2 Principal Cells That Function in Cell-Mediated Immunity
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T Cells and Cellular Immunity
 T cells respond to Ag by T-cell receptors
 T cells require antigen-presenting cells
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Antigen-Presenting Cells
 Digest antigen
 Ag fragments on APC surface with MHC
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T Helper Cells
 T cells
 recognize Ags on APC
 T cells produce cytokines and differentiate into:
 T-cells
 Memory cells
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Figure 17.11 Lineage of effector T helper cell classes and pathogens targeted.
Antibodies
B cell
TH1 cells
TH2 cells
TH17 cells
Recruits neutrophils; provides
protection against extracellular
bacteria and fungi
TH17 cells
TH cell
IL-17
IL-4
IFN-g
Cell-mediated immunity; control
of intracellular pathogens, delayed
hypersensitivity reactions (page
535); stimulates macrophages.
TH1 cells
TH2 cells
Fungi
Extracellular
bacteria
Neutrophil
Macrophage
Mast cell
Basophil
Eosinophil
Intracellular
bacteria and
protozoa
Important in allergic
responses, especially by
production of IgE
Stimulates activity of
eosinophils to control
extracellular parasites
such as helminths (see
ADCC, page 495).
Helminth
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Figure 17.10 Activation of CD4+T helper cells.
An APC encounters and ingests a microorganism. The
antigen is enzymatically processed into short peptides,
which combine with MHC class II molecules and are
displayed on the surface of the APC.
A receptor (TCR) on the surface of the CD4+T helper
cell (TH cell) binds to the MHC–antigen complex. If
this includes a Toll-like receptor, the APC is
stimulated to secrete a costimulatory molecule.
These two signals activate the TH cell, which
produces cytokines.
TH cell receptor
(TCR)
APC (dendritic
cell)
The cytokines cause the TH cell
(which recognizes a dendritic cell
that is producing costimulatory
molecules) to become activated.
T helper cell
Antigen
Microorganism
carrying antigens
Antigen
fragment
(short peptides)
Complex of MHC
class II molecule
and antigen
fragment
Cytokines
Costimulatory molecule,
(required to activate T cells
that have not previously
encountered antigen)
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T Cytotoxic Cells
 or TC cells
 Activated into cytotoxic T lymphocytes (CTLs)
 Induce apoptosis in target cell
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Figure 17.12 Killing of virus-infected target cell by cytotoxic T lymphocyte.
Processed antigen
presented with
MHC class I
Processed
antigen
T cell
receptors
Infected
target cell
is lysed
MHC
class I
Virus-infected cell (example
of endogenous antigen)
A normal cell will not trigger a
response by a cytotoxic T
lymphocyte (CTL), but a virusinfected cell (shown here) or a
cancer cell produces abnormal
endogenous antigens.
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CTL
Virus-infected cell
Cytotoxic T lymphocyte (CTL)
The abnormal antigen is
presented on the cell surface in
association with MHC class I
molecules. CD8+T cells with
receptors for the antigen are
transformed into CTLs.
The CTL induces destruction
of the virus-infected cell by
apoptosis.
Figure 17.13 Apoptosis.
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T Regulatory Cells
 Suppress T cells against self
 Suppress an immune response
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Natural Killer (NK) Cells
 Kill virus-infected and tumor cells
 Attack parasites
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Cytokines
 Chemical messengers
 Overproduction leads to cytokine storm
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Immunological Memory
 Antibody titer is the amount of Ab in serum
 Primary response occurs after initial contact
with Ag
 Secondary (memory or anamnestic)
response occurs after second exposure
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Figure 17.17 The primary and secondary immune responses to an antigen.
Antibody titer in serum
IgG
IgM
Initial
exposure
to antigen
Time (days)
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Second
exposure
to antigen
Types of Adaptive Immunity
 Naturally acquired active immunity
 Resulting from infection
 Naturally acquired passive immunity
 Transplacental or via colostrum
 Artificially acquired active immunity
 Injection of Ag (vaccination)
 Artificially acquired passive immunity
 Injection of Ab
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Terminology of Adaptive Immunity
 Serology: the study of reactions between
antibodies and antigens
 Antiserum: the generic term for serum because it
contains Ab
 Globulins: serum proteins
 Gamma (g) globulin: serum fraction containing the
most Ab
 Immunoglobulins: antibodies
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Chapter
1718
Chapter
Functional
Practical
Applications
Anatomy ofof
Prokaryotic
Immunology
and
Eukaryotic Cells
© 2013 Pearson Education, Inc.
Lectures prepared by Christine L. Case
Chapter 18, unnumbered figure B, page 510, Reported numbers of measles cases in the United States,
1960–2010. (CDC, 2010)
140
Reported number of cases
120
Vaccine
licensed
500,000
450,000
Reported number of cases
400,000
100
80
60
40
20
350,000
0
2000
300,000
01
02
03
04
05
Year
06
07
08
09
10
250,000
200,000
150,000
100,000
50,000
0
1960
1965
1970
1975
1985
1980
Year
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1990
1995
2000
2005
2010
Vaccines Used to Prevent Bacterial
Diseases
Disease
Diphtheria
Vaccine
Purified diphtheria toxoid
Meningococcal
meningitis
Pertussis (whooping
cough)
Pneumococcal
pneumonia
Purified polysaccharide from
Neisseria meningitidis
Inactivated toxin plus acellular
fragments of Bordetella pertussis
Purified polysaccharide from
seven strains of Streptococcus
pneumoniae
Purified tetanus toxoid
Tetanus
Haemophilus influenzae Polysaccharide from Haemophilus
type b meningitis
influenzae type b conjugated with
protein to enhance effectiveness
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Vaccines Used to Prevent Viral
Diseases
Disease
Influenza
Measles
Vaccine
Injected vaccine, inactivated virus
(nasally administered: attenuated
virus)
Attenuated virus
Mumps
Attenuated virus
Rubella
Attenuated virus
Chickenpox
Attenuated virus
Poliomyelitis
Killed virus
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Vaccines Used to Prevent Viral
Diseases
Disease
Vaccine
Rabies
Killed virus
Hepatitis B
Antigenic fragments of virus
Hepatitis A
Inactivated virus
Smallpox
Live vaccinia virus
Herpes zoster
Attenuated virus
Human papillomavirus
Antigenic fragments of virus
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Vaccines for Persons Aged 0–6 Years




Hepatitis B
Rotavirus
DTaP
Haemophilus
influenzae type b
 Pneumococcal
 Inactivated poliovirus
 Influenza
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



MMR
Varicella
Hepatitis A
Meningococcal
Types of Vaccines
 Attenuated whole-agent vaccines- living
pathogens
 MMR vaccine
 Inactivated whole-agent vaccines- dead
pathogens or inactive viruses
 Salk polio vaccine
 Toxoids- inactivated toxins; used against toxin the
pathogen produces
 Tetanus vaccine
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Types of Vaccines
 Subunit vaccines- antigenic fragments
 Acellular pertussis
 Recombinant hepatitis B
 Nucleic acid (DNA) vaccines- plasmids
 West Nile (for horses)
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Figure 18.1 Influenza viruses are grown in embryonated eggs.
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Safety of Vaccines
 No PERFECT vaccine or effects
 Therapeutic index
 Risk-versus-benefit calculation
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