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TORTORA  FUNKE  CASE
ninth edition
MICROBIOLOGY
an introduction
17
Adaptive Immunity:
Specific Defenses
of the Host
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Fig. 16.01
The two arms of the adaptive immune system
Fig. 16.03
Antigen: a molecule (or parts of one) that causes antibody generation
(Immunoglobulin)
The specific region on
an antigen recognized
by an antibody
Fig. 16.04
Antibody Structure
Diversity in antibodies due to variable region
An infinitely large number of possible immunoglobulins;
5 different classes: IgG, IgM, IgA, IgD & IgE
Fig. 16.06
Effects of Antigen-Antibody Interactions
Effects of Antigen-Antibody Interactions-2
Parasites; virally –
infected host cells
NK cells release perforins
and proteases
Fig. 16.09
How is the antibody response triggered?
1. T-cell dependent antigens
2. T-cell independent Ags
e.g. polysaccharides, LPS
response of young
children to these antigens
is poor
Result: Clonal
selection and
expansion of Bcells
Result:
Memory
A plasma cell
Clonal Expansion
Why is the RER in plasma
cells so extensive?
3.
4.
1.
Negative selection
2.
Affinity maturation
Class switching: IgM – IgG—
IgG / IgA
Formation of memory cells
Fig. 16.11
Memory Cells mediate secondary response and lifelong immunity
Cellular Immunity
1. Cytotoxic T cells (CD8+)
• Eliminates cells infected with virus, intracellular parasite
2. Helper T cells (CD4+)
• Mediates B-cell proliferation; macrophage activation
Both stimulated by dendritic cells (cells of innate immunity)
Both produce cytokines that stimulate own proliferation
Fig. 16.20
T cells activated by dendritic cells
A
B
C
Fig. 16.18
A. Recognition of virally-infected cell by cytotoxic T cell
results in apoptosis
B: Helper T-cell activation and interaction with B-cells
Fig. 16.19
C. Helper T- cells can
also activate
macrophages
Activated macrophage: a hungry beast!
•enlarged
•membrane becomes irregular
•increased number of _lysosomes,
containing antimicrobial
substances________
•produce nitric oxide
Terminology
 Antigen (Ag): A substance that causes the body to
produce specific antibodies or sensitized T cells.
 Antibody (Ab): Proteins made in response to an Ag;
can combine with that Ag.
 Complement: Serum proteins that bind to Ab in
an Ag–Ab reaction; cause cell lysis.
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Dual Nature of Adaptive Immunity
 Adaptive immunity develops during an individual’s
lifetime.
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Dual Nature of Adaptive Immunity
 Humoral immunity involves antibodies produced by
B cells.
 B cells recognize antigens by antibodies on their
surfaces.
PLAY
Animation: Humoral Immunity
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Dual Nature of Adaptive Immunity
 Cell-mediated immunity involved T cells.
 T cells recognize antigens by TCRs on their
surfaces.
PLAY
Animation: Cell-Mediated Immunity
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Antigenic Determinants
 Antibodies recognize and react with antigenic
determinants or epitopes on an antigen.
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Figure 17.1
Antibody Structure
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Figure 17.3a–b
IgG antibodies
 Monomer
 80% of serum antibodies
 Fix complement
 In blood, lymph, and intestine
 Cross placenta
 Enhance phagocytosis; neutralize
toxins and viruses; protects fetus
and newborn
 Half-life = 23 days
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Table 17.1 (1 of 3)
IgM Antibodies
 Pentamer
 5-10% of serum antibodies
 Fix complement
 In blood, lymph, and on B
cells
 Agglutinates microbes; first
Ab produced in response
to infection
 Half-life = 5 days
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Table 17.1 (2 of 3)
IgA Antibodies
 Dimer
 10-15% of serum antibodies
 In secretions
 Mucosal protection
 Half-life = 6 days
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Table 17.1 (3 of 3)
IgD Antibodies
 Monomer
 0.2% of serum antibodies
 In blood, lymph, and on B cells
 On B cells, initiate immune
response
 Half-life = 3 days
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Table 17.1 (1 of 3)
IgE Antibodies
 Monomer
 0.002% of serum antibodies
 On mast cells, basophils, and in
blood
 Allergic reactions; lysis of
parasitic worms
 Half-life = 2 days
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Table 17.1 (1 of 3)
Activation of B Cells
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Figure 17.4
Clonal Selection
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Figure 17.5
Activation of B Cells
 T-independent antigen
 T-dependent antigen
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Figure 17.6
T-Dependent Antigens
 Activated TH cell
secretes cytokines
 TH cell recognizes
antigen
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Figure 17.18, step 1
Self-Tolerance
 Body doesn't make Ab against self.
 Clonal deletion
 The process of destroying B and T cells that react to
self antigens.
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The Diversity of Antibodies
 During embryonic development, regions of V genes
combine with C genes to produce  1015 different
antibodies.
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Antigen—Antibody Binding
 Affinity: Strength of bond between Ag and Ag.
 Specificity: Ab recognizes a specific epitope.
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The Results of Ag-Ab Binding
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Figure 17.7
Pathogens entering the gastrointestinal or
respiratory tracts pass through
 M (microfold) cells over
 Peyer’s patches which contain
 Antigen-presenting cells and
 T cells
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T Cells
 Helper T Cells (CD4, TH)
 TCRs: Recognize antigens and MHC II.
 TH1: Activate cells related to cell-mediated immunity
(TOLL).
 TH2: Activate B cells to produce eosinophils, IgM,
and IgE.
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Activation of TH
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Figure 17.9
T Cells
 Cytotoxic T Cells (CD8,
TC) activated in cytotoxic
T lymphocytes.
 CTLs recognize
Ag + MHC I.
 Induce apoptosis
in target cell.
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Figure 17.11
Activation of TC into CTL
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Figure 17.10
T Cells
 Regulatory T Cells (TR)
 Suppress other T cells
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Antigen-Presenting Cells
 Digest antigen
 Ag fragments on APC
surface with MHC
 B cells
 Dendritic Cells
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Figure 17.12
Antigen-Presenting Cells
 Activated macrophages:
Macrophages stimulated
by ingesting Ag or by
cytokines.
PLAY
Animation: Antigen Processing and Presentation
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Figure 17.13
Extracellular Killing
 Antibody-dependent
cells-mediated
cytotoxicity.
 Natural killer cells
destroy cells which
don’t express MHC I.
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Figure 17.14b
Extracellular Killing
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Figure 17.14a
Immune System Cells Communicate
via Cytokines
 Interleukin-1: Stimulates TH cells.
 Interleukin-2: Activates TH, B, TC, and NK cells.
 Interleukin-8: Attracts phagocytes.
 Interleukin-10: Intereferes with TH1 cell activation.
 Interleukin-12: Differentiation of CD4 cells.
 -Interferon: Increase activity of macrophages.
 Chemokines: Cause leukocytes to move to an infection.
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Immunological Memory
 Antibody titer is the amount of Ab in serum.
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 17.15
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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Figure 17.18
•prevent opsonization (Protein A and Fc receptor)
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ii) evade specific immune response (antibodies)
Antigenic variability (phase variation):
alter genes that encode surface proteins
like adhesins
Low immunogenicity:
‘Teflon’ pathogens (spirochaetes)
few surface proteins
IgA protease
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Viral evasion of cytotoxic T cell and NK cell attack
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