17

Adaptive Immunity:
Specific Defenses
of the Host
SLOs
Differentiate between innate and adaptive immunity, and humoral and cellular immunity.
Define antigen, epitope, and hapten.
Explain the function of antibodies and describe their structural and chemical
characteristics. Name one function for each of the five classes of antibodies.
Compare and contrast T-dependent antigens and T-independent antigens.
Differentiate between plasma cell and memory cell.
Describe clonal selection.
Describe how a human can produce different antibodies.
Describe four outcomes of an antigen-antibody reaction.
Differentiate between helper T and cytotoxic T
Define apoptosis.
Define antigen-presenting cell.
Describe the role of antibodies and natural killer cells in antibody-dependent cell-
mediated cytotoxicity.
Identify at least one function of each of the following: cytokines, interleukins, interferons.
Distinguish a primary from a secondary immune response.
Contrast the four types of adaptive immunity.
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 Immune System Overview
Innate immunity: An individual’s genetically
predetermined resistance to certain diseases.
Adaptive immunity: Ability of the body to react to
specific microbial infection.
Adaptive immunity
● is antigen specific, has memory
● is made up of two branches
Humoral Immunity (B cell mediated)
Cellular Immunity (T cell mediated)
● collaborates with innate immunity
● has ability to ignore healthy “self” molecules
(tolerance)
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 Vocabulary
● 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.
● Serology: The study of reactions between
antibodies and antigens.
● Antiserum: A generic term for serum because it
contains Ab.
● Globulins: Serum proteins
● Immunoglobulins (= Gamma ( ) globulins): Serum
antibodies
● Complement:
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Serum Proteins

Fig 17.18
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The Nature of Antigens
Antigens and
antigenic
Determinants

Antibodies
recognize and
react with
antigenic
determinants or
epitopes on an
antigen
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Haptens Fig 17.2

Definition: Small separable part of an antigen that

reacts specifically with an antibody but is incapable
of stimulating antibody production except in
combination with a carrier protein molecule

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 The Nature of Antibodies
Immunoglobulin Structure: 4 polypeptide chains (2
heavy and 2 light)
Fig 17.3
● Variable regions
● Constant regions

Copyright © 2010 Pearson Education, Inc. Fig 17.3

IgG antibodies
● Monomer
● 80% of serum antibodies
● Activate 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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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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IgA Antibodies
● Dimer
● 10-15% of serum
antibodies
● In secretions
● Mucosal protection
● Half-life = 6 days

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 IgD Antibodies IgE Antibodies
● Monomer ● Monomer
● 0.2% of serum ● 0.002% of serum
antibodies antibodies
● In blood, lymph, and on● On mast cells,
B cells basophils, and in blood
● On B cells, initiate ● Allergic reactions; lysis
immune response of parasitic worms
● Half-life = 3 days ● Half-life = 2 days

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 B cells and Humoral Immunity
Effective against free antigen (toxins, bacterial
surface structures, viruses in between cells)
B cell receptors (mostly IgM and IgD)
Activated B-cells go through clonal expansion
leading to
Plasma cells (effector cell for
antibody production) and
Memory cells

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Clonal Selection

Fig 17.5

ANIMATION Humoral Immunity: Clonal Selection and Expansion

Response to T – dependent antigens
B cells require help of T cells for most protein
antigens (T-dependent ag)
B cells internalize antigen and present it to T-
helper cell in combination with MHC class II
molecules
If T cell recognizes antigen it
activates B cell clonal expansion
plasma cells and memory cells

Review Fig
17.4
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Antigen
Presentation by
B-cell

Compare to Fig. 17.4

Response to T – Independent Antigens

No T-helper cells involved

Polysaccharides (bacterial capsules) and LPS

Weak response
with no memory
cells
Young children
react poorly
Fig 17.6
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Antibody Diversity

1015 different B-cell receptors

How many genes in human genome?
Mechanism of antibody diversity: somatic
Susumu Tonegawa
Nobel Prize 1987
recombination
(during embryonic development)
Primarily through Gene rearrangement (mix
and match)
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Antigen—Antibody Binding and its Results
Affinity: Strength of bond between Ag and Ag.
Specificity: Ab recognizes a specific epitope.
Antibody function:
agglutinate and precipitate
opsonize
neutralize (immobilize and prevent adherence)
activate complement
Antibody-Dependent Cell-mediated Cytotoxicity
(ADCC) via NK cells and eosinophils
Protective outcome disposal of antigen
(based on antigen-antibody binding)
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 The Results
of Ag-Ab
Binding

Fig 17.7

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 T Cells and Cellular Immunity
Compare to
T cells have TCR on Fig 17.10
surface.
TCR does not recognize
free antigen. Ag must
be presented in
association with MHC
on an antigen-
presenting cell (APC).
Antigens are processed
by APC and positioned
on the surface of the
APC.
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 APCs
● Digest antigen
● Ag fragments on APC
surface with MHC-II
● B cells
● Dendritic Cells
● Macrophages
● Activated macrophages:
Macrophages stimulated
by ingesting Ag or by
cytokines.

ANIMATION Cell-Mediated Immunity: Helper T Cells

Classes of T cells
Helper T Cells (CD4, TH)
are activated by antigen presented by MHC class II.
After binding to Ag presented by APC, CD4 cells
secrete cytokines activating other T cells and B cells
TH1 cells activate cells involved in cellular immunity
TH2 stimulate production of eosinophils, IgM, and IgE
( associated with allergic reactions and parasitic
infections)
Cytotoxic T cells (CD8, TC, CTL)
activated by endogenous antigens and MHC class I
When activated transform into CTLs and memory cells
CTLs lyse target cell or induce apoptosis
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MHC Class I on all
nucleated cells

Antigen
Recognition by
T Cells

MHC Class II on
surface of APCs
(Macrophages, B-
cells, dendritic cells)
 Mechanism of Destruction of cells
Action of CTL displaying MHC-I-Ag
complexes  

Perforin molecules
create protein channels
in target cell membrane

Granzymes enter and trigger

apoptosis in target cell
Similar but different
from MAC !!
Compare to Fig.
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Education, Inc.
Natural Killer (NK) Cells
Granular leukocytes.
Not immunologically specific.
Lyse virus-infected and tumor cells.
Kill target cell in absence of MHC-I (early stages of
virus infection and tumor cells)
Similar mechanism to CTLs
In Antibody-Dependent Cell Mediated
Cytotoxicity (ADCC) NK cells and macrophages
lyse antibody-coated cells (protozoans and
helminths)
Fig 17.15
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 Immunological Memory
● Amount of antibody in serum is called the antibody titer.
● 1 response: Response of the body to the first contact
with an antigen. Mostly IgM
● 2 response: any subsequent contact with the same
antigen. Rapidly very high antibody titer. Mostly IgG

Fig 17.16

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 Self Tolerance: Negative Selection

Goal: eliminate B and T cells, recognizing “self”

molecules
Clonal deletion of B cells taking place in bone
marrow apoptosis
Negative selection of T cells in thymus
Failure results in auto-antibodies and
autoimmune disease

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 Types of Specific Immunity
Active immunity
Protection via introduction of antigen into
responsive host, e.g.:
Naturally acquired via infection
or
Artificially acquired via
vaccination

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 Passive Immunity
Protection via transfer of antibodies or
immune cells into a non-immune host, e.g.:

Naturally acquired:
Fetus receives mothers
antibodies via placenta
Artificially acquired via
vaccination injection of
immune serum after
exposure (snake bite,
Rh+ child with Rh-
mother etc.)
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Compare to
Fig 17.17
 Cellular Immunity Review

T-cells specific surface receptors (TCRs)

TCR cannot bind free ag. Ag must be
presented by APCs
Activated T-cells go through clonal expansion
effector and memory T cells.
CTLs directly kill virus infected and tumor
cells
T-helper cells help the humoral and cellular
immunity

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The