Adaptive-Immunity.ppt adaptive type of immunity

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
PowerPoint® Lecture Slide Presentation prepared by Christine L. Case
M I C R O B I O L O G Y
a n i n t r o d u c t i o n
ninth edition TORTORA  FUNKE  CASE
17
Adaptive Immunity:
Specific Defenses
of the Host

Adaptive Immunity:
Specific Defenses of the Host
 Innate immunity: Defenses against any pathogen.
 Adaptive immunity: Specific antibody and lymphocyte
response to an antigen.

Historical Development
 Pasteur observed immunity in chickens injected with
weakened pathogens.
 Von Behring received the Nobel Prize for development
of antitoxin.
 Ehrlich’s work led to the identification of antibodies
in serum.

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.

Antigens
 Mostly protein or large polysaccharides, E.g. capsules,
cell walls, flagella, fimbriae, toxins of bacteria, coats of
viruses or bacterial surfaces
 Nonmicrobial substances include pollen, egg white,
serum protein, transplanted tissues or organs
 With molecular weight of 10,000 or higher

Dual Nature of Adaptive Immunity
 Adaptive immunity develops during an individual’s
lifetime.

 Humoral immunity involves antibodies produced by
B cells.
 B cells recognize antigens by antibodies on their
surfaces.
PLAY Animation: Humoral Immunity

 Cell-mediated immunity involved T cells.
 T cells recognize antigens by TCRs on their
surfaces.
PLAY Animation: Cell-Mediated Immunity

Terminology
 Serology: The study of reactions between antibodies
and antigens.
 Antiserum: The generic term for serum because it
contains Ab.
 Globulins: Serum proteins
 Immunoglobulins: Antibodies
 Gamma () globulin: Serum fraction containing Ab.

Serum Proteins
Figure 17.17

Antigenic Determinants
 Antibodies recognize and react with antigenic
determinants or epitopes on an antigen.
Figure 17.1

Haptens
 React with antibodies.
 How is this different from an antibody?
Figure 17.2

Antibody Structure
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
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
Table 17.1 (2 of 3)

IgA Antibodies
 Dimer
 10-15% of serum antibodies
 In secretions
 Mucosal protection
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
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
Table 17.1 (1 of 3)

Activation of B Cells
Figure 17.4

Clonal Selection
Figure 17.5

Activation of B Cells
 T-independent antigen
 T-dependent antigen
Figure 17.6

T-Dependent Antigens
Figure 17.18, step 1
 Activated TH cell
secretes cytokines
 TH cell recognizes
antigen

Self-Tolerance
 Body doesn't make Ab against self.
 Clonal deletion
 The process of destroying B and T cells that react to
self antigens.

The Diversity of Antibodies
 During embryonic development, regions of V genes
combine with C genes to produce  1015 different
antibodies.

Antigen—Antibody Binding
 Affinity: Strength of bond between Ag and Ag.
 Specificity: Ab recognizes a specific epitope.

The Results of Ag-Ab Binding
Figure 17.7

 M (microfold) cells over
 Peyer’s patches which contain
 Antigen-presenting cells and
 T cells
Pathogens entering the gastrointestinal or
respiratory tracts pass through

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.

Activation of TH
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.
Figure 17.11

Activation of TC into CTL
Figure 17.10

T Cells
 Regulatory T Cells (TR)
 Suppress other T cells

Antigen-Presenting Cells
 Digest antigen
 Ag fragments on APC
surface with MHC
 B cells
 Dendritic Cells
Figure 17.12

Antigen-Presenting Cells
 Activated macrophages:
Macrophages stimulated
by ingesting Ag or by
cytokines.
Figure 17.13
PLAY Animation: Antigen Processing and Presentation

Extracellular Killing
 Antibody-dependent
cells-mediated
cytotoxicity.
 Natural killer cells
destroy cells which
don’t express MHC I.
Figure 17.14b

Extracellular Killing
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.

Immunological Memory
 Antibody titer is the amount of Ab in serum.
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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