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Chapter 21A
Immune System:
Innate and Adaptive Defenses
Slides by Barbara Heard and W. Rose.
figures from Marieb & Hoehn 9th ed.
Portions copyright Pearson Education
Nobel Prizes for Immune System Discoveries
2011 Beutler, Hoffmann, Steinman, "for their discoveries
concerning the activation of innate immunity”; “for his discovery
of the dendritic cell and its role in adaptive immunity”
[H: Toll receptors in fruit
flies essential for innate
immunity. B: Found Tolllike receptors in
mammals & clarified
their important role in
innate immunity. S:
Discovered dendritic
cells & showed they
have special ability to
present antigens to &
activate naïve T cells.
Langerhans cells in skin
Dead fruit fly with fungus growing on it because it has mutant
are a subtype of DCs.]
Toll receptors. …&Hoffman, Cell, 1996.
Nobel Prizes for Immune System Discoveries
1996 Doherty, Zinkernagel
“for their discoveries concerning the specificity of the cell
mediated immune defence”
[Discovered that killer T cells recognize virus-infected cells by
simultaneous recognition of self & non-self markers. Explains
benefits of HLA, which is a barrier to organ transplant.]
1987 Susumu Tonegawa
"for his discovery of the genetic principle for generation of
antibody diversity“
[how to make millions of antibodiy proteins from a small
number of genes by genetic shuffling]
Nobel Prizes for Immune System Discoveries
1984 Jerne, Köhler, Milstein
"for theories concerning the specificity in development
and control of the immune system and the discovery of
the principle for production of monoclonal antibodies"
[Jerne: we are born with a full repertoire of antibodies
and select the needed ones when we encounter a new
pathogen. K. & M.: fused lymphocytes with tumor cells
to create immortal cells (hybridomas) that make one
antibody specifically]
Nobel Prizes for Immune System Discoveries
1980 Benacerraf, Dausset, Snell
"for their discoveries concerning genetically
determined structures on the cell surface that regulate
immunological reactions“
[discovery & understanding of MHC (HLA in humans)]
1972 Edelman, Porter
"for their discoveries concerning the chemical structure
of antibodies“
[Y shape, heavy & light chains, constant & variable
regions]
Nobel Prizes for Immune System Discoveries
1960 Burnet, Medawar
"for discovery of acquired immunological tolerance“
[Burnet: “immunological tolerance”; both showed how
early immune system cells become self-tolerant]
1930 Landsteiner
"for his discovery of human blood groups"
[blood groups and blood typing]
1919 Bordet
"for his discoveries relating to immunity"
[antigens and antibodies]
Nobel Prizes for Immune System Discoveries
1913 Richet
"in recognition of his work on anaphylaxis“
[Discovered & coined term for anaphylaxis &
elucidated how it occurs.]
1908 Mechnikov, Ehrlich
"in recognition of their work on immunity"
[Mechinov discovered & coined the term phagocytosis
& phagocytes; Erlich discovered antibodies]
Nobel Prizes for Immune System Discoveries
1901 von Behring
"for his work on serum therapy, especially its
application against diphtheria, by which he has opened
a new road in the domain of medical science and
thereby placed in the hands of the physician a
victorious weapon against illness and deaths“
[von Behring discovered that when animals were
injected with tiny doses of weakened forms of tetanus
or diphtheria bacteria, their blood extracts contained
chemicals released in response, which rendered the
pathogens' toxins harmless.]
Immune System: Links to articles
Treating allergies with pills instead of shots NYT 20131206
The case against cleanliness: a skeptical review NYT 20120910
The boy with a thorn in his joints NYT 20130301 An interesting and
moving article by a mother about her son, his juvenile idiopathic arthritis, and
alternative medicine. Interesting comments too.
Immunity
• Resistance to disease
• Immune system
– Two intrinsic systems
• Innate (nonspecific) defense system
• Adaptive (specific) defense system
© 2013 Pearson Education, Inc.
Immune System
• Functional system rather than organ
system
• Innate and adaptive defenses intertwined
• Release and recognize many of same
defensive molecules
• Innate defenses do have specific
pathways for certain substances
• Innate responses release proteins that
alert cells of adaptive system to foreign
molecules
© 2013 Pearson Education, Inc.
Immunity
• Innate defense system has two lines of
defense
– First - external body membranes (skin and
mucosae)
– Second - antimicrobial proteins, phagocytes,
and other cells
• Inhibit spread of invaders
• Inflammation most important mechanism
© 2013 Pearson Education, Inc.
Immunity
• Adaptive defense system
– Third line of defense attacks particular foreign
substances
• Takes longer to react than innate system
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Figure 21.1 Overview of innate and adaptive defenses.
Surface barriers
• Skin
• Mucous membranes
Innate
defenses
Internal defenses
• Phagocytes
• Natural killer cells
• Inflammation
• Antimicrobial proteins
• Fever
Humoral immunity
• B cells
Adaptive
defenses
Cellular immunity
• T cells
© 2013 Pearson Education, Inc.
Innate Defenses
• Surface barriers ward off invading
pathogens
– Skin, mucous membranes, and their
secretions
• Physical barrier to most microorganisms
• Keratin resistant to weak acids and bases,
bacterial enzymes, and toxins
• Mucosae provide similar mechanical barriers
© 2013 Pearson Education, Inc.
Surface Barriers
• Protective chemicals inhibit or destroy
microorganisms
– Acidity of skin and secretions – acid mantle –
inhibits growth
– Enzymes - lysozyme of saliva, respiratory
mucus, and lacrimal fluid – kill many
microorganisms
– Defensins – antimicrobial peptides – inhibit
growth
– Other chemicals - lipids in sebum, dermcidin
in sweat – toxic
© 2013 Pearson Education, Inc.
Surface Barriers
• Respiratory system modifications
– Mucus-coated hairs in nose
– Cilia of upper respiratory tract sweep dustand bacteria-laden mucus toward mouth
• Surface barriers breached by nicks or cuts
- second line of defense must protect
deeper tissues
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Internal Defenses: Cells and Chemicals
• Necessary if microorganisms invade
deeper tissues
– Phagocytic cells
– Natural killer (NK) cells
– Antimicrobial proteins (interferons and
complement proteins)
– Fever
– Inflammatory response (macrophages, mast
cells, WBCs, and inflammatory chemicals)
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Phagocytic cells
• Neutrophils most abundant but die fighting
– Become phagocytic on exposure to infectious
material
• Macrophages develop from monocytes – chief
phagocytic cells
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Mechanism of Phagocytosis
• Phagocyte must adhere to particle
– Some microorganisms evade adherence with
capsule
• Opsonization marks pathogens—coating by
complement proteins or antibodies
• Cytoplasmic extensions bind to and engulf
particle in vesicle
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Figure 21.2a Phagocytosis.
Innate defenses
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Internal defenses
A macrophage (purple) uses its cytoplasmic
extensions to pull rod-shaped bacteria
(green) toward it. Scanning electron
micrograph (4800x).
Figure 21.2b Phagocytosis.
1 Phagocyte
adheres to
pathogens or debris.
Phagosome
(phagocytic
vesicle)
Lysosome
Acid
hydrolase
enzymes
2 Phagocyte forms
pseudopods that
eventually engulf the
particles, forming a
phagosome.
3 Lysosome fuses
with the phagocytic
vesicle, forming a
phagolysosome.
4 Lysosomal
enzymes digest the
particles, leaving a
residual body.
5 Exocytosis of the
vesicle removes
indigestible and
residual material.
Events of phagocytosis.
© 2013 Pearson Education, Inc.
Slide 1
Mechanism of Phagocytosis
• Pathogens killed by acidifying and digesting with
lysosomal enzymes
• Helper T cells cause release of enzymes of
respiratory burst, which kill pathogens resistant
to lysosomal enzymes by
– Releasing cell-killing free radicals
– Producing oxidizing chemicals (e.g., H2O2)
– Increasing pH and osmolarity of phagolysosome
• Defensins (in neutrophils) pierce membrane
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Natural Killer (NK) Cells
• Nonphagocytic large granular lymphocytes
• Attack cells that lack "self" cell-surface
receptors
– Induce apoptosis in cancer cells and virusinfected cells
• Secrete potent chemicals that enhance
inflammatory response
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Inflammatory Response
•
•
•
•
•
Triggered whenever body tissues injured
Prevents spread of damaging agents
Disposes of cell debris and pathogens
Alerts adaptive immune system
Sets the stage for repair
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Inflammatory Response
• Cardinal signs of acute inflammation:
1. Redness
2. Heat
3. Swelling
4. Pain
(Sometimes 5. Impairment of function)
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Inflammatory Response
• Begins with chemicals released into ECF
by injured tissues, immune cells, blood
proteins
• Macrophages and epithelial cells of
boundary tissues bear Toll-like receptors
(TLRs)
• 11 types of TLRs recognize specific
classes of infecting microbes
• Activated TLRs trigger release of
cytokines that promote inflammation
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Inflammatory Response
• Inflammatory mediators
– Kinins, prostaglandins (PGs), and
complement
• Dilate local arterioles (hyperemia)
– Causes redness and heat of inflamed region
• Make capillaries leaky
• Many attract leukocytes to area
• Some have inflammatory roles
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Inflammatory Response: Edema
•  Capillary permeability  exudate to
tissues
– Fluid containing clotting factors and
antibodies
– Causes local swelling (edema)
– Swelling pushes on nerve endings  pain
• Pain also from bacterial toxins, prostaglandins, and
kinins
– Moves foreign material into lymphatic vessels
– Delivers clotting proteins and complement
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Inflammatory Response
• Clotting factors form fibrin mesh
– Scaffold for repair
– Isolates injured area so invaders cannot
spread
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Figure 21.3 Inflammation: flowchart of events.
Innate defenses
Internal defenses
Initial stimulus
Physiological response
Tissue injury
Release of inflammatory chemicals
(histamine, complement,
kinins, prostaglandins, etc.)
Signs of inflammation
Result
Release of leukocytosisinducing factor
Leukocytosis
(increased numbers of white
blood cells in bloodstream)
Arterioles
dilate
Increased capillary
permeability
Local hyperemia
(increased blood
flow to area)
Capillaries
leak fluid
(exudate formation)
Leaked protein-rich
fluid in tissue spaces
Heat
Redness
Locally increased
temperature increases
metabolic rate of cells
Pain
Attract neutrophils,
monocytes, and
lymphocytes to
area (chemotaxis)
Margination
(leukocytes cling to
capillary walls)
Leaked clotting
proteins form interstitial
clots that wall off area
to prevent injury to
surrounding tissue
Swelling
Possible temporary
impairment of
function
Temporary fibrin
patch forms
scaffolding for repair
Healing
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Leukocytes migrate to
injured area
Diapedesis
(leukocytes pass through
capillary walls)
Phagocytosis of pathogens
and dead tissue cells
(by neutrophils, short-term;
by macrophages, long-term)
Pus may form
Area cleared of debris
Phagocyte Mobilization
• Neutrophils lead; macrophages follow
– As attack continues, monocytes arrive
• 12 hours after leaving bloodstream 
macrophages
• These "late-arrivers" replace dying neutrophils and
remain for clean up prior to repair
• If inflammation is due to pathogens,
complement will be activated; cells of
adaptive immunity will arrive
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Phagocyte Mobilization
• Steps for phagocyte mobilization
1. Leukocytosis: release of neutrophils from
bone marrow in response to leukocytosisinducing factors from injured cells
2. Margination: neutrophils cling to walls of
capillaries in inflamed area in response to
CAMs
3. Diapedesis of neutrophils
4. Chemotaxis: inflammatory chemicals
(chemotactic agent) promote positive
chemotaxis of neutrophils
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Figure 21.4 Phagocyte mobilization.
Innate defenses
Internal defenses
Inflammatory
chemicals
diffusing
from the
inflamed
site act as
chemotactic
agents.
1 Leukocytosis.
Neutrophils enter
blood from bone
marrow.
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Slide 1
2 Margination.
Neutrophils cling
to capillary wall.
4 Chemotaxis.
Neutrophils follow
chemical trail.
Capillary wall
Basement
membrane
Endothelium
3 Diapedesis.
Neutrophils flatten
and squeeze out of
capillaries.
Antimicrobial Proteins
• Include interferons and complement
proteins
• Some attack microorganisms directly
• Some hinder microorganisms' ability to
reproduce
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Interferons
• Family of immune modulating proteins
– Have slightly different physiological effects
• Viral-infected cells secrete IFNs (e.g., IFN
alpha and beta) to "warn" neighboring
cells
– IFNs enter neighboring cells  produce
proteins that block viral reproduction and
degrade viral RNA
– IFN alpha and beta also activate NK cells
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Interferons
• IFN gamma (immune interferon)
– Secreted by lymphocytes
– Widespread immune mobilizing effects
– Activates macrophages
• Since IFNs activate NK cells and
macrophages, indirectly fight cancer
• Artificial IFNs used to treat hepatitis C,
genital warts, multiple sclerosis, hairy cell
leukemia
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Figure 21.5 The interferon mechanism against viruses.
Innate defenses
Slide 1
Internal defenses
Virus
Viral nucleic acid
1 Virus
New viruses
enters cell.
2 Interferon
genes switch
on.
5 Antiviral
proteins
block viral
reproduction.
Antiviral
mRNA
DNA
Nucleus
mRNA for
interferon
3 Cell
produces
interferon
molecules.
Interferon
receptor
Host cell 1
Infected by virus;
makes interferon;
is killed by virus
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Interferon
Host cell 2
Binds interferon
from cell 1; interferon
induces synthesis of
protective proteins
4 Interferon binding
stimulates cell to
turn on genes for
antiviral proteins.
Complement System (Complement)
• ~20 blood proteins that circulate in inactive
form
• Include C1–C9, factors B, D, and P, and
regulatory proteins
• Major mechanism for destroying foreign
substances
• Our cells contain complement activation
inhibitors
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Complement
• Unleashes inflammatory chemicals that
amplify all aspects of inflammatory
response
• Kills bacteria and certain other cell types
by cell lysis
• Enhances both innate and adaptive
defenses
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Complement Activation
• Three pathways to activation
– Classical pathway
• Antibodies bind to invading organisms and to
complement components
• Called complement fixation
• First step in activation; more details later
– Lectin pathway
– Alternative pathway
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Complement
Lectin pathway
Lectins: proteins produced by liver
Some bind to mannose (sugar) residues found
on surface of many pathogens.
When lectin binds, it can activate other proteins
in the complement pathway.
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Complement
Alternative pathway
Complement system is in a continuous low level
of activation
Complement regulatory proteins on host cells
(i.e. our own cells) keep complement system in
check
Many pathogens lack complement regulatory
proteins, so their presence allows complement
to become activated
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Complement Activation
• Each pathway involves activation of
proteins in an orderly sequence
• Each step catalyzes the next
• Each pathway converges on C3, which
cleaves into C3a and C3b
• Common terminal pathway initiated that
– Enhances inflammation, promotes
phagocytosis, causes cell lysis
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Complement Activation
• Cell lysis begins when
– C3b binds to target cell  insertion of complement
proteins called membrane attack complex (MAC)
into cell's membrane
– MAC forms and stabilizes hole in membrane  influx
of water  lysis of cell
• C3b also causes opsonization
• C3a and other cleavage products amplify
inflammation
– Stimulate mast cells and basophils to release
histamine
– Attract neutrophils and other inflammatory cells
© 2013 Pearson Education, Inc.
Figure 21.6 Complement activation.
Classical pathway
Activated by antibodies
coating target cell
Lectin pathway
Activated by lectins
binding to specific sugars
on microorganism’s surface
Alternative pathway
Activated spontaneously. Lack of
inhibitors on microorganism’s
surface allows process to proceed
Together with other complement
proteins and factors
C3
C3a
C3b
MACs form from activated
complement components (C5b
and C6–C9) that insert into the
target cell membrane, creating
pores that can lyse the target cell.
C3b
C5b
MAC
Opsonization:
Coats pathogen
surfaces, which
enhances phagocytosis
C6
C7
C8
C9
C5a
Enhances inflammation:
Stimulates histamine
release, increases blood
vessel permeability,
attracts phagocytes by
chemotaxis, etc.
Pore
Complement
proteins
(C5b–C9)
Membrane
of target cell
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Fever
• Abnormally high body temperature
• Systemic response to invading
microorganisms
• Leukocytes and macrophages exposed to
foreign substances secrete pyrogens
• Pyrogens act on body's thermostat in
hypothalamus, raising body temperature
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Fever
• Benefits of moderate fever
– Causes liver and spleen to sequester iron and
zinc (needed by microorganisms)
– Increases metabolic rate  faster repair(?)
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Adaptive Defenses
• Adaptive immune (specific defense)
system
– Protects against infectious agents and
abnormal body cells
– Amplifies inflammatory response
– Activates complement
– Must be primed by initial exposure to specific
foreign substance
• Priming takes time
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Adaptive Defenses
• Specific – recognizes and targets specific
antigens
• Systemic – not restricted to initial site
• Have memory – stronger attacks to
"known" antigens
• Two separate, overlapping arms
– Humoral (antibody-mediated) immunity
– Cellular (cell-mediated) immunity
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Humoral Immunity
• Antibodies, produced by lymphocytes,
circulating freely in body fluids
• Bind temporarily to target cell
– Temporarily inactivate
– Mark for destruction by phagocytes or
complement
• Humoral immunity has extracellular targets
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Cellular Immunity
• Lymphocytes act against target cell
– Directly – by killing infected cells
– Indirectly – by releasing chemicals that
enhance inflammatory response; or activating
other lymphocytes or macrophages
• Cellular immunity has cellular targets
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Antigens
• Antibody Generators
• Substances that can mobilize adaptive
defenses and provoke an immune
response
• Targets of all adaptive immune responses
• Most are large, complex molecules not
normally found in body (nonself)
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Complete Antigens
• Important functional properties
– Immunogenicity: ability to stimulate
proliferation of specific lymphocytes
– Reactivity: ability to react with activated
lymphocytes and antibodies released by
immunogenic reactions
• Examples: foreign protein,
polysaccharides, lipids, and nucleic acids
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Haptens (Incomplete Antigens)
• Small molecules (haptens) not
immunogenic by themselves
– E.g., peptides, nucleotides, some hormones
• May be immunogenic if attached to body
proteins and combination is marked
foreign
• Cause immune system to mount harmful
attack
• Examples: poison ivy, animal dander,
detergents, and cosmetics
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Antigenic Determinants
• Only certain parts (antigenic
determinants) of entire antigen are
immunogenic
• Antibodies and lymphocyte receptors bind
to them as enzyme binds substrate
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Antigenic Determinants
• Most naturally occurring antigens have
numerous antigenic determinants that
– Bind to different antibodies
– Mobilize several different lymphocyte
populations
• Large, chemically simple molecules (e.g.,
plastics) have little or no immunogenicity
© 2013 Pearson Education, Inc.
Figure 21.7 Most antigens have several different antigenic determinants.
Antigenbinding
sites
Antibody A
Antigen
Antibody B
Antibody C
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Antigenic determinants
Self-antigens: MHC Proteins
• Protein molecules (self-antigens) on
surface of cells not antigenic to self but
antigenic to others in transfusions or grafts
• Example: MHC glycoproteins
– Coded by genes of major histocompatibility
complex (MHC) and unique to individual
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Cells of the Adaptive Immune System
– Two types of lymphocytes
• B lymphocytes (B cells)—humoral immunity
• T lymphocytes (T cells)—cellular immunity
– Antigen-presenting cells (APCs)
• Do not respond to specific antigens
• Play essential auxiliary roles in immunity
© 2013 Pearson Education, Inc.
Figure 21.8 Lymphocyte development, maturation, and activation.
Adaptive defenses
Primary lymphoid organs
(red bone marrow and thymus)
Humoral immunity
Cellular immunity
Secondary lymphoid organs
(lymph nodes, spleen, etc.)
Red bone marrow
1 Origin
• Both B and T lymphocyte precursors originate in red
bone marrow.
Lymphocyte
precursors
2 Maturation
• Lymphocyte precursors destined to become T cells migrate
(in blood) to the thymus and mature there.
• B cells mature in the bone marrow.
• During maturation lymphocytes develop immunocompetence
and self-tolerance.
Thymus
Red bone marrow
Antigen
Lymph node
3 Seeding secondary lymphoid organs and circulation
• Immunocompetent but still naive lymphocytes leave the
thymus and bone marrow.
• They “seed” the secondary lymphoid organs and circulate
through blood and lymph.
4 Antigen encounter and activation
• When a lymphocyte’s antigen receptors bind its antigen, that
lymphocyte can be activated.
5 Proliferation and differentiation
• Activated lymphocytes proliferate (multiply) and then
differentiate into effector cells and memory cells.
• Memory cells and effector T cells circulate continuously in
the blood and lymph and throughout the secondary
lymphoid organs.
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Slide 1
Maturation
• "Educated" to become mature; B cells in
bone marrow, T cells in thymus
– Immunocompetence – lymphocyte can
recognize one specific antigen by binding to it
• B or T cells display only one unique type of antigen
receptor on surface when achieve maturity – bind
only one antigen
– Self-tolerance
• Lymphocytes unresponsive to own antigens
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T cells
• T cells mature in thymus under negative
and positive selection pressures ("tests")
– Positive selection
• Selects T cells capable of recognizing self-MHC
proteins (MHC restriction); failures destroyed by
apoptosis
– Negative selection
• Prompts apoptosis of T cells that bind to selfantigens displayed by self-MHC
• Ensures self-tolerance
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Figure 21.9 T cell education in the thymus.
Adaptive defenses
Cellular immunity
1. Positive Selection
T cells must recognize self major histocompatibility
proteins (self-MHC)
AntigenDeveloping
presenting
T cell
thymic cell
Failure to recognize selfMHC results in apoptosis
(death by cell suicide).
T cell receptor
Self-MHC
Self-antigen
Recognizing self-MHC
results in survival.
Survivors proceed
to negative selection.
2. Negative Selection
T cells must not recognize self-antigens
Recognizing self-antigen
results in apoptosis. This
eliminates self-reactive
T cells that could cause
autoimmune diseases.
Failure to recognize (bind
tightly to) self-antigen
results in survival and
continued maturation.
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B cells
• B cells mature in red bone marrow
• Positively selected if successfully make
antigen receptors
• Those that are self-reactive
– Eliminated by apoptosis (clonal deletion)
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Seeding Secondary Lymphoid Organs and
Circulation
• Immunocompetent B and T cells not yet
exposed to antigen called naive
• Move from primary lymphoid organs (bone
marrow and thymus) to "seed" secondary
lymphoid organs (lymph nodes, spleen,
etc.)
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Antigen Encounter and Activation
• Clonal selection
– Naive lymphocyte's first encounter with
antigen  selected for further development
– If correct signals present, lymphocyte will
complete its differentiation
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Proliferation and Differentiation
• Activated lymphocyte proliferates  exact
clones
• Most clones  effector cells that fight
infections
• A few remain as memory cells
– Able to respond to same antigen more quickly
second time
• B and T memory cells and effector T cells
circulate continuously
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Antigen Receptor Diversity
• Genes, not antigens, determine which
foreign substances immune system will
recognize
– Immune cell receptors result of acquired
knowledge of microbes likely in environment
• Lymphocytes make a billion or more
different types of antigen receptors
– Coded for by ~1,000 genes
– Gene segments are shuffled by somatic
recombination
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Table 21.3 Overview of B and T Lymphocytes
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Antigen-presenting Cells (APCs)
• Engulf antigens
• Present fragments of antigens to T cells
for recognition
• Major types
– Dendritic cells in connective tissues and
epidermis
– Macrophages in connective tissues and
lymphoid organs
– B cells
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Dendritic Cells and Macrophages
• Dendritic cells phagocytize pathogens,
enter lymphatics to present antigens to T
cells in lymph node
– Most effective antigen presenter known
– Key link between innate and adaptive
immunity
• Macrophages widespread in lymphoid
organs and connective tissues
– Present antigens to T cells to activate
themselves into voracious phagocytes that
secrete bactericidal chemicals
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Adaptive Immunity: Summary
• Uses lymphocytes, APCs, and specific
molecules to identify and destroy nonself
substances
• Depends upon ability of its cells to
– Recognize antigens by binding to them
– Communicate with one another so that whole
system mounts specific response
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Activation and Differentiation of B Cells
• B cell activated when antigens bind to its
surface receptors
• Causes proliferation and differentiation
into effector cells (mostly plasma cells, a
few memory B cells)
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Fate of the Clones
• Most clone cells become plasma cells
– Secrete specific antibodies at rate of 2000
molecules per second for four to five days,
then die
– Antibodies circulate in blood or lymph
• Bind to free antigens and mark for destruction by
innate or adaptive mechanisms
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Fate of the Clones
• Clone cells that do not become plasma
cells become memory B cells
– Provide immunological memory
– Allow stronger, faster response to future
exposures to same antigen
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Figure 21.11a Clonal selection of a B cell.
Adaptive defenses
Humoral immunity
Primary response
(initial encounter
with antigen)
Activated B cells
Plasma cells
(effector B cells)
Secreted
antibody
molecules
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Proliferation to
form a clone
Antigen
Antigen binding
to a receptor on a
specific B lymphocyte
(B lymphocytes with
noncomplementary
receptors remain
inactive)
Memory B cell—
primed to respond
to same antigen
Immunological Memory
• Primary immune response
– Cell proliferation and differentiation upon first
antigen exposure
– Lag period: three to six days
– Peak levels of plasma antibody are reached in
10 days
– Antibody levels then decline
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Immunological Memory
• Secondary immune response
– Re-exposure to same antigen gives faster,
more prolonged, more effective response
• Sensitized memory cells respond within hours
• Antibody levels peak in two to three days at much
higher levels
• Antibodies bind with greater affinity
• Antibody level can remain high for weeks to
months
© 2013 Pearson Education, Inc.
Figure 21.11 Clonal selection of a B cell.
Adaptive defenses
Humoral immunity
Primary response
(initial encounter
with antigen)
Activated B cells
Proliferation to
form a clone
Plasma cells
(effector B cells)
Memory B cell—
primed to respond
to same antigen
Secreted
antibody
molecules
Secondary response
(can be years later)
Antigen
Antigen binding
to a receptor on a
specific B lymphocyte
(B lymphocytes with
noncomplementary
receptors remain
inactive)
Clone of cells
identical to
ancestral cells
Subsequent
challenge by same
antigen results in
more rapid response
Plasma
cells
Secreted
antibody
molecules
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Memory
B cells
Figure 21.12 Primary and secondary humoral responses.
Secondary immune response to
antigen A is faster and larger; primary
immune response to antigen B is
similar to that for antigen A.
Antibody titer (antibody concentration)
in plasma (arbitrary units)
Primary immune
response to antigen
A occurs after a delay.
104
103
102
101
100
0
7
First exposure
to antigen A
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AntiBodies
to B
AntiBodies
to A
14
21
28
35
42
Second exposure to antigen A;
first exposure to antigen B
Time (days)
49
56
Active Humoral Immunity
• When B cells encounter antigens and
produce specific antibodies against them
• Two types of active humoral immunity:
– Naturally acquired—response to bacterial or
viral infection
– Artificially acquired—response to vaccine of
dead or attenuated pathogens
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Active Humoral Immunity
• Vaccines
– Most of dead or attenuated pathogens
– Spare us symptoms of primary response
– Provide antigenic determinants that are
immunogenic and reactive
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Passive Humoral Immunity
• Readymade antibodies introduced into
body
• B cells are not challenged by antigens
• Immunological memory does not occur
• Protection ends when antibodies degrade
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Passive Humoral Immunity
•
Two types
1. Naturally acquired—antibodies delivered to
fetus via placenta or to infant through milk
2. Artificially acquired—injection of serum,
such as gamma globulin
•
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Protection immediate but ends when antibodies
naturally degrade in body
Figure 21.13 Active and passive humoral immunity.
Humoral
immunity
Active
Naturally
acquired
Infection;
contact
with
pathogen
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Artificially
acquired
Vaccine;
dead or
attenuated
pathogens
Passive
Naturally
acquired
Antibodies
passed from
mother to
fetus via
placenta; or
to infant in
her milk
Artificially
acquired
Injection of
exogenous
antibodies
(gamma
globulin)