CHAPTER 8
Adaptive Immunity
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General Characteristics of
Adaptive Immunity
■ Works together with inflammation.
■ Recognizes foreign or “nonself” substances.
– Antigens
■ Pathogens
■ Noninfectious environmental agents
■ Drugs
■ Vaccines
■ Transfusions
■ Transplants
■ Provides long-term protection.
■ Is slower than innate but more specific.
■ Has memory.
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General Characteristics of
Adaptive Immunity (Cont.)
■ End products of adaptive immunity
– Lymphocytes: T and B cells
– Antibodies: Immunoglobulins (Ig)
■ Generation of clonal diversity
– Each individual T or B cell specifically recognizes
only one particular antigen.
– Sum of the population of lymphocyte specificities
may represent millions of foreign antigens.
– Primary lymphoid organs: Is the thymus for T
cells and bone marrow for B cells.
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General Characteristics of
Adaptive Immunity (Cont.)
■ Clonal diversity
– Occurs in primary lymphoid organs.
– Involves the maturing of B and T cells.
– Migrates to secondary lymphoid organs.
■ Clonal selection
– Antigen is processed and presented to immune
cells by antigen-presenting cells (APCs).
– Cellular interaction of T-helper cells (Th) and
APCs
■ Results in the differentiation of B cells into
active antibody-producing cells (plasma cells)
and T cells into effector cells.
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4
General Characteristics of
Adaptive Immunity (Cont.)
■ Clonal diversity and selection
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5
Humoral and Cellular Immunity
■ Humoral immunity
– B cells and circulating antibodies are the primary cells.
– Causes direct inactivation of a microorganism or the
activation of inflammatory mediators.
– Primarily protects against bacteria and viruses.
■ Cellular immunity
– Differentiates T cells.
– Primarily protects against viruses and cancer.
■ Humoral and cellular immunity work together to provide
immunity and memory.
– Respond more rapidly and efficiently on subsequent
exposure to the same antigen.
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Humoral and Cellular Immunity
(Cont.)
Type of Immunity
Primary Cells
Functions
Protection
Humoral
B cells and circulating Causes direct inactivation Protects against
antibodies
of a microorganism or the
bacteria and
activation of inflammatory
viruses.
mediators.
Cell-mediated
T cells
T-cell differentiation
Kills targets directly,
or stimulates the
activity of other
leukocytes.
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Protects against
viruses and cancer.
7
Active vs. Passive Immunity
Active Immunity—
Active Acquired
Immunity
Passive Immunity—
Passive Acquired
Immunity
•Antibodies or T cells
are produced after
either
a natural exposure to
an antigen or after
immunization.
•Is long lived.
•Preformed antibodies
or T lymphocytes are
transferred from a
donor to a recipient.
•Occurs naturally
or artificially.
•Is temporary or shortlived.
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8
Active vs. Passive Immunity
Question 1
Which statement indicates the nurse has an accurate understanding
concerning passive immunity?
Passive immunity
1. “is produced after exposure to an antigen.”
2. “is the result of an attenuated immunization.”
3. “can last for years.”
4. “can be transferred from a donor to a recipient.”
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9
Recognition and Response
■ Recognition and response are required for a successful
immune response.
■ Are complicated processes and involve a highly effective
interaction of cells.
■ Cluster of differentiation (CD)
– Originally, CD was used to describe proteins found on
the surface of lymphocytes.
– Currently, CD is a labeling system used to identify a
family of proteins on many cells.
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Antigen
■ Is a molecule that can react with antibodies or receptors on
B and T cells.
■ Is mostly protein but can be other molecules as well.
■ Immunogenic antigen: An antigen that can trigger an
immune response
■ Sites for binding to antibodies and lymphocytes
– Antigen’s binding site: antigenic determinant (epitope)
– Antibody or lymphocyte’s binding site: Antigen-binding
site (paratope)
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Antigen (Cont.)
■ Degree to which an antigen has immunogenic capability.
– Degree of foreignness to a host
■ Is most important.
– Size
■ If large is extremely immunogenic.
■ Small–molecular-weight antigens are called haptens:
Cannot trigger the immune response themselves but
can when bound to a carrier protein.
– Chemical complexity
■ The greater the diversity, the more the
immunogenicity.
– Amount
■ High or low extremes can cause tolerance.
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Antigen (Cont.)
■ Tolerance: We recognize ourselves as not foreign.
– Central tolerance: Lymphocytes with receptors
against self-antigens are eliminated.
– Peripheral tolerance: Prevents recognition by
lymphocytes and antibodies.
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Molecules that Recognize
Antigens
■ Types
– Circulating antibody
– Antigen receptors on B cells or B-cell
receptors (BCR)
– Antigen receptors on T lymphocytes or T-cell
receptors (TCR)
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Antibody
■ Is also called immunoglobulin (Ig).
■ Is produced by plasma cells.
■ Has several classes
– IgG, IgA, IgM, IgE, and IgD
■ Are characterized by antigenic, structural,
and functional differences.
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Antibody (Cont.)
■ IgG
– Is the most abundant class (80% to 85%).
– Is transported across the placenta.
– Accounts for most of the protective activity
against infections.
– Four classes: IgG1, IgG2, IgG3, and IgG4.
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Antibody (Cont.)
■ IgA
– Has two subclasses.
■ IgA1 molecules: Are predominantly in the
blood.
■ IgA2 molecules: Are predominantly in
normal body secretions.
– IgAs in body secretions are dimers anchored
by
the J-chain and “secretory piece.”
■ Secretory piece may function to protect
IgAs against enzyme degradation.
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Antibody (Cont.)
■ IgA secretory immune system
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Antibody (Cont.)
■ IgM
– Is the largest of the immunoglobulins.
– Pentamer is stabilized by a J-chain.
– Is the first antibody produced during a response
to an antigen.
– Is synthesized during fetal life.
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Antibody (Cont.)
■ IgD
– Information on IgD function is limited.
– Concentration is low in the blood.
– Is located primarily on the surface of
developing
B lymphocytes.
– Functions as one type of B-cell antigen
receptor.
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Antibody (Cont.)
■ IgE
– Is the least concentrated of the
immunoglobulin classes in the circulation.
– Acts as a mediator of many common allergic
responses.
– Defends against parasites.
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Antibody (Cont.)
Antibody
IgG
IgA
IgE
IgD
General
Information
Most prevalent
Mostly in
secretions
Most rare
Functions
Most of
protective
activity against
infection.
Most of
protective
activity in body
secretions.
Mediator of Functions as First
many
one type of antibody
common
B-cell
produced
allergic
antigen
during the
responses. receptor.
initial, or
primary,
Defends
response to
against
an antigen.
parasitic
Crosses the
placenta.
Not well known
IgM
Largest
infections.
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Antibody
Question 2
Which information is most correct regarding IgAs?
IgAs are
1. measureable in the blood in very low
concentrations.
2. the largest immunoglobulins.
3. found in saliva and other body secretions.
4. effective against parasites and allergies.
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Antibody Molecular Structure
■ Antigen-binding fragment (Fab)
– Acts as recognition sites (receptors) for antigenic
determinants; binds antigen; has two identical
fragments.
■ Crystalline fragment (Fc)
– Is responsible for biologic function.
■ Activates complement and opsonization.
■ Polypeptide chains (four)
– Two light chains and two heavy chains are held
together with disulfide bonds.
■ Heavy chain determines the type of antibody.
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Antigen Binding
■ Amino acid sequences of the variable regions
of the heavy and light chains
■ Framework regions that control antibody folding
■ Lock and key
– Noncovalent chemical interactions
■ Antibody valence (number of binding sites)
– IgG, IgD, circulating IgA and IgE—2
– Secretory IgA—4
– IgM—theoretically 10, likely 5
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B Cell–Receptor Complex
■ Is located on the surface of B cells.
■ Consists of
– Antigen-recognition molecules
■ Membrane-associated IgM and IgD
■ Responsible for recognition and binding
– Accessory intracellular-signaling molecules
■ Ig-alpha and Ig-beta heterodimers
■ Responsible for sending message to mature and
to make antibodies
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T Cell–Receptor Complex
■ Consists of
– Antibody-like transmembrane protein
(TCR)
■ Responsible for recognition and
binding.
– Accessory proteins for intracellular
signaling
■ Are referred to as CD3.
■ Are responsible for sending message
to activate and differentiate T cells.
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Molecules that Present Antigen
■ Are needed for an effective immune
response.
■ Antigen is processed within cells.
■ Are expressed on the cell surface in a
specific manner.
■ Some antigens need special APCs;
others can be processed by most any
type of cell.
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Molecules that Present Antigen (Cont.)
■ Major histocompatibility complex (MHC)
– Glycoproteins on the surface of all human cells
(except red blood cells [RBCs])
– Human leukocyte antigens (HLA) alleles:
Inherited in a codominant fashion to enable both
maternal and paternal antigens to be expressed
– Are also called HLAs
– MHC class I genes: A, B, and C
– MHC class II genes: DR, DP, and DQ
– MHC class III genes: Other genes that control
the quality and quantity of an immune response
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Transplantation
■ Cells in transplanted tissue from one
individual have a different set of MHC
surface antigens than those of the recipient.
■ The recipient can mount an immune
response against foreign MHC molecules.
■ The more similar two individuals are in HLA
tissue type, the more likely for a successful
transplant.
■ Haplotype: Is a specific combination of
alleles at the six major HLA loci on one
chromosome (A, B, C, DR, DQ, and DP).
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CD1
■ Antigen-presenting molecules
■ Found on APCs and thymus cells.
■ Present lipid antigens
– Mycobacterium tuberculosis
– Mycobacterium leprae
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Molecules that Hold Cells
Together
■ Antigen-independent interactions
between cells
■ Resulting in intracellular signaling events
that are independent of the TCR or BCR
complexes
■ Necessary complement to antigenspecific signaling
■ Needed for effective immune response
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Cytokines and Their Receptors
■ Low–molecular-weight proteins or glycoproteins,
function as chemical signals between cells.
■ Are secreted by APCs and lymphocytes.
■ Results
– Cytokines increase the production of
proteins.
– Lymphocytes proliferate and differentiate.
– A combination of cytokines influences a
given cell that ultimately determines that
cell’s response.
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Generation of Clonal Diversity
■ All necessary receptor specificities are
produced.
■ Takes place in the primary (central)
lymphoid organs.
– Thymus for T cells, bone marrow for B
cells
■ Results in immature but
immunocompetent
T and B cells.
■ Migrates to secondary lymphoid organs to
wait for antigens.
■ Primarily occurs in the fetus.
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Generation of Clonal Diversity
(Cont.)
■ Usually beings at birth and proceeds throughout
life.
■ Rearrangement of smaller regions of DNA during
T- and B-cell development
■ DNA loci that encode immunoglobulins and TCRs
are rearranged
– Somatic recombination
– Each cell is unique and able to react with different
antigens.
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B-Cell Maturation
■ Occurs in the bone marrow.
■ Stem cell matures.
■ Develops surface markers.
– Interleukin (IL)–7 receptor
■ IL-7: Is produced by stromal cells; is critical in driving
the further differentiation and proliferation of the B
cell.
■ Production of BCRs
– Heavy and light chains
– Light: V, J, and C genes
– Heavy: V, D, and J genes
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B-Cell Maturation (Cont.)
■ Changes in characteristic surface markers
– CD21: Complement receptor
– CD40: Adhesion molecule required for later
interactions with Th cells
■ Central tolerance
– Large number of autoreactive B cells are eliminated if
exposed to self-antigen—over 90%.
■ Peripheral tolerance
– Autoreactive B cell clones persist and must be
controlled by other means in the lymphoid organs.
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T-Cell Maturation
■ Thymus is the central lymphoid organ of T-cell
development.
■ T cells move from the thymic cortex to the medulla.
■ Changes include the development of the TCRs and
the expression of surface molecules.
■ T cells are released into the blood and take up
residence in the secondary lymph organs to await
antigens.
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T-Cell Maturation (Cont.)
■ Production of TCRs
– Contains α- and β-chains, each of which has
a variable region and a constant region.
■ Complementary-determining regions
(CDRs) separated by framework regions
(FRs) are within each V region.
■ V region genes
■ Joining (J) region genes
– Sequence for the development of α- and βchains are different.
– Allows for the identification of many antigens.
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T-Cell Maturation (Cont.)
■ Produces changes in characteristic surface markers.
– Initiates the expression of CD2 on the cell surface.
■ CD2 is a marker for T cells.
– Developing T cells make surface proteins CD4 and
CD8.
– CD4 cells recognize antigens presented by MHC
class II molecules and develop into T-helper cells.
– CD8 cells recognize antigens presented by MHC
class I molecules and become mediators of cellmediated immunity and directly kill other cells
(T-cytotoxic [Tc] cells).
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T-Cell Maturation (Cont.)
■ Central tolerance
– Autoreactive T cells in the thymus are deleted.
– Clonal deletion: A TCR strongly reacts with MHC class I
or class II; the T cell will undergo apoptosis.
– Negative selection: Developing T cell’s TCR binds
strongly with a self-antigen causing T cell to be deleted.
– Positive selection: Surface CD4 molecules bind to MHC
class II molecules and become CD4 single–positive;
surface CD8 reacts with MHC class I molecules and
become CD8 single–positive.
■ This positive selection process results in about 60% of
immunocompetent T cells being CD4+ and 40% being
CD8+.
■ Can also have peripheral tolerance.
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Clonal Selection
■ Second phase of the immune response
■ Produces effector cells (Th, plasma, and Tc cells)
and memory cells.
■ Induction of population of T-helper cells
■ Induction of immunocompetent B cells into
plasma cells and immunocompetent CD8+ T
cells into T-cytotoxic cells
■ Begins at birth and proceeds throughout life.
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Secondary Lymphoid
Organs
■ Include the spleen, lymph nodes, adenoids,
tonsils, Peyer patches (intestines), and
appendix.
■ High endothelial venules: Lymphocytes bind to
the endothelium through adhesion molecules.
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Secondary Lymphoid Organs (Cont.)
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Antigen Processing and
Presentation
■ Antigens require processing and presentation by APCs.
– Dendritic cells, macrophages, B lymphocytes
■ B lymphocytes: Present antigen to Th cells that facilitate humoral
immune response.
■ Macrophages: Present antigen to memory Th cells to initiate a
rapid response to antigens (secondary immune response).
■ Dendritic cells: Process antigen from a site of inflammation to Tcell–rich areas of lymph nodes.
– For processing and presentation to occur, antigen must be
the appropriate type, lymphocytes must recognize presented
antigen, and antigen must be appropriately presented.
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Antigen Processing and
Presentation (Cont.)
■ Antigens require processing and presentation by APCs
(cont.)
– Antigen processing: Is the process by which
exogenous and endogenous antigens are linked with
the appropriate MHC molecules.
■ Pathways of antigen processing
– Class I MHC molecules: Generally present
endogenous (inside cells) antigens.
– Class II MHC molecules: Prefer exogenous (outside
cells) antigens.
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T-Helper Lymphocytes
■ Th cells help the antigen-driven maturation of B and T
cells.
■ Facilitate and magnify interaction between APCs and
immunocompetent lymphocytes.
■ Steps
– Th cells interact through antigen-specific and antigenindependent receptors.
– Th cells undergo differentiation.
– Mature Th cells interact with plasma or T-effector
cells.
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T-Helper Lymphocytes
(Cont.)
■ APC-Th cooperation
– Complex of an antigenic peptide presented by an
MHC class II molecule is recognized by multiple
molecules on the Th-cell surface—CD4 (Th) is class II
restricted.
– Costimulatory molecules are necessary for proper
differentiation to occur.
■ B7 on the APC and CD28 on the Th cell: Most
important
■ CD48 on the APC and CD2 on the Th cell
– IL-2 is needed for a Th cell to mature into a
functioning cell.
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T-Helper Lymphocytes
(Cont.)
■ Subsets
– Th1 cells provide help in developing cell-mediated
immunity.
■ Activate macrophages and Tc cells.
– Th2 cells provide help in developing humoral
immunity.
■ Activate B cells.
– Th17 helps the inflammatory response.
– Treg cells limit immune response
– Differences are based on cytokine production.
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T-Helper Lymphocytes
(Cont.)
■ Subsets (cont.)
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B-Cell Clonal Selection
■ Results from the recognition of soluble antigen by
BCRs, processing of antigen, and presentation by
MHC class II antigens to Th2 cells.
■ When an immunocompetent B cell encounters an
antigen for the first time, B cells with specific BCRs
are stimulated to differentiate and proliferate.
■ A differentiated B cell becomes a plasma cell.
■ A plasma cell is a factory for antibody production.
–
Single class or subclass of antibody
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Primary and Secondary
Immune Responses
■ Primary immune response
– Occurs during the initial exposure.
– During the latent period or lag phase, B-cell
differentiation occurs.
– After 5–7 days, an IgM antibody for a specific antigen
is detected.
– An IgG response equal to or slightly less follows the
IgM response.
– The immune system is primed.
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Primary and Secondary
Immune Responses (Cont.)
■ Secondary (anamnestic) immune response
– Is more rapid than the primary response.
– Larger amounts of antibody are produced.
– Rapidity is due to the presence of memory cells that
do not have to differentiate.
– IgM is produced in similar quantities to the primary
response, but IgG is produced in considerably greater
numbers.
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Primary and Secondary
Immune Responses (Cont.)
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Primary and Secondary
Immune Responses
Question 3
Which information is correct regarding the secondary immune
response?
1. A latent period or lag phase occurs.
2. IgM is the primary immunoglobulin.
3. IgG is significantly increased.
4. Memory cells have to develop.
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Cellular Interactions
■ TCR can only “see” processed and presented antigen.
■ BCR can react with soluble antigens.
– Signals originate from the BCR complex and other
surface co-receptors.
– Antigen-bearing macromolecule is eventually
presented on the cell surface and recognized by a
Th2 cell.
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Class Switch
■ Is also called the isotype switch.
■ B cells use IgM and IgD as receptors.
■ During clonal selection, B cells can change antibody class.
– One of four IgGs, one of two IgAs, IgE, or an IgM
– DNA rearrangement (cut then mended)
– CD40-CD40L interaction is needed
■ T-independent antigens
– Bypass Th cells and directly stimulate B cells—cannot
stimulate class switch.
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Class Switch (Cont.)
■ Class switch of B cells
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Cellular Differentiation
■ B cells differentiate into antibody-producing plasma cells
and into long-lived memory cells.
– On reexposure, memory cells do not require much
further differentiation and will rapidly differentiate into
new plasma cells.
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T-Cell Activation
■ Initiates cellular immune response.
■ Binds antigen to TCRs.
■ Allows
– Direct killing of foreign or abnormal cells
(Tc cells or cytotoxic T lymphocytes [CTLs])
– Assistance or activation of other cells
■ T-regulatory cells (Treg)
– Regulate the immune response to avoid attacking “self.”
■ T-memory cells
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T-Cell Activation (Cont.)
■ Cellular interactions
– Recognize antigen that has been processed and
presented by MHC class I molecules or CD8 T cells are
class I restricted.
– Appropriate signaling pathways are needed for the
maturation of T cells.
■
■
■
■
■
■
B7 on the cell-presenting antigen
CD28 on the T cell
CD48 on the APC
CD2 on the T cell
Variety of other adhesion molecules
Requires cytokines, especially IL-2, produced by Th-1 cell.
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T-Cell Activation (Cont.)
■ Cellular differentiation
– Produces active Tc cells with the capacity to identify
antigens on the surface of infected or malignant cells
and then to destroy these cells.
– Produces memory T cells.
■ Have the capacity to respond rapidly if further exposure
to the same antigen occurs.
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T-Cell Activation (Cont.)
■ Superantigens
– These molecules are not digested and processed by
an APC.
– Result in the activation of large populations of
T lymphocytes, regardless of antigen specificity.
– Induce an excessive production of cytokines.
■ Results in a systemic inflammatory reaction, including
fever, low blood pressure, and, potentially, fatal shock.
– Examples
■ Bacterial toxins from Staphylococcus aureus and
Streptococcus pyogenes and some viruses.
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Antibody Function
■ Protects against infection.
■ Direct
– Neutralization: Inactivates or blocks the binding of an
antigen to a receptor.
– Agglutination: Clumps insoluble particles in
suspension.
– Precipitation: Makes a soluble antigen into an
insoluble precipitate.
■ Indirect
– Complement and phagocytes
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Antibody Function (Cont.)
■
Neutralization
– Inactivates or blocks the binding of an antigen to a
receptor by covering the receptor.
– Some vaccinations that have been attenuated
(weakened, inactivated) work this way.
– Antibody titer: Is the level of circulating antibodies.
– Toxoids: Bacterial toxins are chemically inactivated
but still retain immunogenicity.
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Antibody Function (Cont.)
■ Indirect effects
– Is mediated by the Fc portion of the antibody
molecule.
– Includes opsonic activity, leading to enhanced
phagocytosis.
– Activates the complement system, which may lead to
complement-mediated destruction of the pathogen.
– Increases opsonic activity through the deposition of
C3b.
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Secretory (Mucosal) Immune Response
■ Lymphoid tissues protect external body surfaces.
■ Antibodies are present in tears, sweat, saliva, mucus, and breast
milk.
■ Secretory immunoglobulins act locally.
■ Major function
– Is to halt viral and bacterial invasion before local or systemic
disease develops; to prevent a carrier state.
■ IgA is the dominant immunoglobulin.
– Small numbers of IgG and IgM are present.
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Immunoglobulin E (IgE)
■ Is a special class of antibody that protects against large
parasitic worms.
■ Is also the primary cause of allergies.
■ Eosinophil: Is the primary cell for granuloma formation
around the parasite.
– Causes degranulation of the parasite.
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Killing Abnormal Cells
■ Tc lymphocytes
– Destroy cancer cells or cells infected with a virus.
– Induce apoptosis.
■ Perforin: Penetrates, polymerizes, and forms pores in
the target cell’s plasma membrane.
■ Granzymes: Enter target cell through the perforin-lined
pores, and activate cellular enzymes (caspases) that
are involved in apoptosis.
■ Direct receptor interactions: Activation of Fas signals
the target cell to undergo apoptosis.
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Killing Abnormal Cells (Cont.)
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Other Cells that Kill Abnormal
Cells
■ Natural killer (NK) cells
– Are a complement to Tc cell mechanisms.
– Do not undergo maturation in the thymus and lack antigenspecific receptors.
– Kill abnormal cells that do not express MHC class I.
– Antibody-dependent cell-mediated cytotoxicity
■ NK cells can attach to the IgG through Fc receptors and activate
its normal killing mechanisms.
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Other Cells that Kill Abnormal
Cells Question 4
A nurse is asked about NK cells. How should the nurse
respond?
NK cells
1. only work alone to cause apoptosis.
2. destroy abnormal cells with MHC class I
markers.
3. lack antigen-specific receptors.
4. mature in the thymus.
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T Cells that Activate
Macrophages
■ Chronic inflammation: T cells produce cytokines that
activate macrophages.
■ Stimulate a macrophage to become a more efficient
phagocyte.
■ Increase production of proteolytic enzymes and other
antimicrobial substances.
■ Retain macrophages at the inflammatory site.
■ Increase adhesion between Th1 and macrophages.
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T-Regulatory Lymphocytes
■ Tregs suppress immune responses.
– Decrease Th1 and Th2 activity, and suppress antigen
recognition and Th cell proliferation.
■ Provide peripheral tolerance.
■ Control or limit the immune response to protect the host’s
own tissues against autoimmune reactions.
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Fetal and Neonatal
Immune Function
■ Newborns have a poorly developed immune response.
■ Antibody function of the newborn is deficient.
– Is capable of primary IgM response, but is unable to
produce an IgG challenge.
■ Immunity is provided by maternal antibodies.
– Trophoblastic cells transport maternal IgG across the
placenta.
– Newborn IgG levels are near adult levels.
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Fetal and Neonatal
Immune Function (Cont.)
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Aging and Immune Function
■ Decreased T-cell activity
– Thymic size is 15% of its maximum size.
■ Decreased production of specific antibodies
■ Decreased circulating memory B cells
■ Increased circulating immune complexes
■ Increased circulating autoantibodies
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