ninth edition

TORTORA FUNKE CASE

MICROBIOLOGY
an introduction

17
Adaptive Immunity: Specific Defenses of the Host
PowerPoint Lecture Slide Presentation prepared by Christine L. Case
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Adaptive Immunity: Specific Defenses of the Host

Innate immunity: Defenses against any pathogen. Adaptive immunity: Specific antibody and lymphocyte response to an antigen.

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Historical Development
Pasteur observed immunity in chickens injected with weakened pathogens. Von Behring received the Nobel Prize for development of antitoxin.

Ehrlichs work led to the identification of antibodies

in serum.

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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 AgAb reaction; cause cell lysis.

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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

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Dual Nature of Adaptive Immunity

Adaptive immunity develops during an individuals 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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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.

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Serum Proteins

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Figure 17.17

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

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Figure 17.1

Haptens
React with antibodies.

How is this different from an antibody?

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Figure 17.2

Antibody Structure

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Figure 17.3ab

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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AntigenAntibody 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 Peyers 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

Figure 17.13

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Extracellular Killing
Antibody-dependent cells-mediated cytotoxicity. Natural killer cells

destroy cells which

dont 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.

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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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Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Figure 17.18