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Immune System: Overview
• The immune system has three types of components
• Lymphoid tissues
• Various types of immune cells
• Chemical signals that coordinate responses
Copyright © 2010 Pearson Education, Inc.
Immune System: Functions
• Protects against pathogens
• Bacteria
• Viruses
• Parasites
• Protects against foreign molecules (e.g., toxins)
• Removes dead or damaged cells
• Attempts to recognize and remove abnormal cells
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Immune System: Pathologies
• Incorrect immune responses
• Autoimmune disease (e.g., Type 1 diabetes)
• Overactive immune responses
• Allergies
• Lack of immune response
• Immunodeficiency disease (e.g., SCID and AIDS)
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Immunity: Two Intrinsic Defense Systems
• Innate system responds quickly and consists of:
• First line of defense – skin and mucosae prevent entry of
microorganisms
• Second line of defense – antimicrobial proteins, phagocytes,
and other cells
• Inhibit spread of invaders throughout the body
• Inflammation is its most important mechanism
• Adaptive defense system
• Third line of defense – mounts attack against particular foreign
substances
• Takes longer to react than the innate system
• Works in conjunction with the innate system
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Innate and Adaptive Defenses
First line
Second line
Third line
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Figure 21.1
Number of active immune cells
Neutrophils
Macrophages
Natural
killer cells
Plasma cells
Cytotoxic
T cells
Time (weeks)
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Antibody
titer
Figure 22-11 Innate Defenses (Part 1 of 2)
Innate Defenses
Physical barriers
keep hazardous
organisms and
materials outside
the body.
Duct of eccrine
sweat gland
Hair
Secretions
Epithelium
Phagocytes
engulf pathogens
and cell debris.
Fixed
macrophage
Neutrophil
Free
macrophage Eosinophil
Monocyte
Immunological
surveillance
is the destruction of
abnormal cells by NK
cells in peripheral tissues.
Natural
killer cell
Lysed
abnormal
cell
Interferons
are chemical messengers
that coordinate the
defenses against viral
infections.
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Interferons released by activated
lymphocytes, macrophages, or
virus-infected cells
Figure 22-11 Innate Defenses (Part 2 of 2)
Innate Defenses
Complement
system
consists of circulating
proteins that assist
antibodies in the
destruction of pathogens.
Lysed
pathogen
Complement
Inflammatory
response
is a localized, tissue-level
response that tends to
limit the spread of an
injury or infection.
Mast cell
1. Blood flow increased
2. Phagocytes activated
3. Capillary permeability increased
4. Complement activated
5. Clotting reaction walls off region
6. Regional temperature increased
7. Adaptive defenses activated
Fever
is an elevation of body
temperature that accelerates
tissue metabolism and the
activity of defenses.
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Body temperature rises above 37.2ºC in
response to pyrogens
First line of defense: Surface Barriers
• Skin, mucous membranes, and their secretions make
up the first line of defense
• Keratin in the skin:
• Presents a physical barrier to most microorganisms
• Is resistant to weak acids and bases, bacterial
enzymes, and toxins
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First line of defense: Epithelial Barriers
• Epithelial membranes produce protective chemicals that destroy
microorganisms
• Skin acidity (pH of 3 to 5) inhibits bacterial growth
• Sebum contains chemicals toxic to bacteria
• Stomach mucosae secrete concentrated HCl and proteindigesting enzymes
• Saliva and lacrimal fluid contain lysozyme
• Mucus traps microorganisms that enter the digestive and respiratory
systems
• Mucus-coated hairs in the nose trap inhaled particles
• Mucosa of the upper respiratory tract is ciliated
• Cilia sweep dust- and bacteria trapped by mucus away from
lower respiratory passages
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Second line of defense: Cells and Chemicals
• The body uses nonspecific cellular and chemical
devices to protect itself
• Phagocytes and natural killer (NK) cells
• Antimicrobial proteins in blood and tissue fluid
• Inflammatory response enlists macrophages, mast
cells, WBCs, and chemicals
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Second line of defense: Phagocytes
• Macrophages are the main phagocytic cells
• Two general types:
• Macrophages – most derived from monocytes
• Fixed (ex. Kupffer cells in liver)
• Free/mobile - wander throughout a region in
search of cellular debris
• Microphages
eosinophils
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–
circulating
neutrophils
and
Figure 21.2a
Second line of defense: Phagocytes
• Neutrophils become phagocytic when encountering
infectious material
• Eosinophils are weakly phagocytic against parasitic
worms
• Mast cells bind and ingest a wide range of bacteria
• Mast cells are found in the connective tissue and
are similar to basophiles
• Originate in the bone marrow
• contain special cytoplasmic granules which store
mediators of inflammation
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Phagocytes Ingest Foreign Material
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Figure 24-4 (2 of 4)
1 Microbe adheres to phagocyte.
2 Phagocyte forms pseudopods that
eventually engulf the particle.
Lysosome
Phagocytic vesicle
containing antigen
(phagosome).
3 Phagocytic vesicle is
fused with a lysosome.
Phagolysosome
Acid
hydrolase
enzymes
4 Microbe in fused vesicle
is killed and digested by
lysosomal enzymes within
the phagolysosome, leaving
a residual body.
Residual body
5 Indigestible and
residual material
is removed by
exocytosis.
(b)
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Figure 21.2b
Second line of defense: Inflammation
• The inflammatory response is triggered whenever body
tissues are injured
• Prevents the spread of damaging agents to nearby
tissues
• Disposes of cell debris and pathogens
• Initiate repair processes
• The four signs of acute inflammation are
• Swelling
• Redness
• Heat
• Pain
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Inflammation Response
• Begins with chemical “alarm”
• a flood of inflammatory chemicals released into
the extracellular fluid
• Macrophages and epithelial cells of boundary
tissues have Toll-like receptors (TLRs)
• TLRs recognize specific classes of infecting
microbes
(even
though
we
consider
macrophages to be “non-specific”)
• Activated TLRs trigger the release of cytokines
that promote inflammation and attract WBC
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Inflammatory Response
• Some of the inflammatory mediators
• Histamine – amino acid derivative produced by basophiles and
must cell- promote vasodilation
• Kinins – plasma proteins that are activated by tissue injury and
promote vasodilation
• prostaglandins (PGs) – promote neutrophil diapedesis
• Leukotrienes – stimulate vasodilation and netrophil cemotaxis
• Complement – set of proteins that promote phgocytosis, activates
cells of the immune system
• Colony-Stimulating Factors – hormones that promote WBC
count
• Cells that are involved
• WBC, helper T cells, platelets, endothelial cells
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Five Steps of Inflammation
1. Macrophages engulf debris and foreign matter
2. Capillaries dilate and become more permeable
3. Foreign matter contained
4. More leukocytes migrate to area
5. Leukocytes clear infection
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1. Phagocytosis of Pathogens
• Proteins on microbes bound by macrophages
• Triggers phagocytosis and secretions
• Secretory products trigger subsequent steps
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2. Dilation and Increased Permeability in Capillaries
• Damaged mast cells secrete histamine
• Histamine triggers dilation and increases
permeability
• Result: increased blood flow and increased
movement of proteins and cells to injured tissue
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2. Vasodilation and Increased Vascular Permeability
• The most immediate requirement is to bring WBC to the
injury site!
• Vasodilation – causes hyperemia (increased blood
flow) (Which sign of inflammation?)
• Increase permeability of blood walls (cells separate
slightly) – causes edema (leakage of exudate) (Which
sign of inflammation?)
• Exudate—fluid containing proteins, clotting factors, and
antibodies
• Exudate moves into tissue spaces causing local edema
(swelling), which contributes to the sensation of pain
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3. Containment of Foreign Matter
• Clotting factors eventually form clot in tissue,
prevents spread of foreign matter
• Eventually forms a scab
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4. Inflammatory Response: Phagocytic Mobilization
• Four main phases:
• Leukocytosis – neutrophils are released from the bone
marrow in response to leukocytosis-inducing factors released
by injured cells
• Margination – neutrophils cling to the walls of capillaries in
the injured area
• Endothelial cells in the injury site produce cell-adhesion
molecules that make the surface “sticky” to help in this
process
• Diapedesis – neutrophils squeeze through capillary walls and
begin phagocytosis
• Chemotaxis – inflammatory chemicals attract neutrophils to
the injury site
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4. Leukocyte Migration and Proliferation
• 1 hour: neutrophil migration
• 10 hours: monocyte migration  macrophages
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Fever
• Abnormally high body temperature in response to invading
microorganisms
• Maintenance of a body temperature above 37.2oC (99oF)
• The body’s thermostat is reset upwards in response to pyrogens,
chemicals secreted by leukocytes and macrophages exposed to
bacteria and other foreign substances
• High fevers are dangerous because they can denature enzymes
• Moderate fever can be beneficial:
• Promotes INF activity
• May inhibit some viruses and bacteria reproduction
• Increase body metabolism so enzymatic reactions occur faster
and so is tissue repair
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Second line of defense: Antimicrobial Proteins
• Enhance the innate defenses by:
• Attacking microorganisms directly
• Interfering with microorganisms’ ability to reproduce
• The most important antimicrobial proteins are:
• Interferon
• Complement proteins
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Second line of defense: Interferons – defense against viruses
• Interferons (INF) provide rapid response.
• Produced by a variety of body cells
• Lymphocytes produce gamma (), or immune, interferon
• Most other WBCs produce alpha () interferon
• Fibroblasts produce beta () interferon
• INF alpha and beta are the most potent against viruses
• All three interferons increase expression of class I MHC
molecules and thus promote recognition by cytotoxic T cells.
• All three interferons can activate NK cells which can then
kill virus-infected cells.
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Figure 22-13 Interferons
Alpha ()-interferons are
produced by cells infected
with viruses. They attract
and stimulate NK cells and
enhance resistance to viral
infection.
Beta ()-interferons,
secreted by fibroblasts,
slow inflammation in a
damaged area.
Gamma ()-interferons,
secreted by T cells and NK
cells, stimulate
macrophage activity.
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Second line of defense: Interferon (IFN)
• when a host cell is invaded by a virus it activates the genes
that synthesize IFN
• Interferon molecules leave the infected cell and enter
neighboring cells
• Interferon stimulates the neighboring cells to activate
genes for PKR (an antiviral protein)
• PKR nonspecifically blocks viral reproduction in the
neighboring cell
• Interferons also activate macrophages and mobilize NKs
• Interferon can not save the infected cell but can
prevent the virus from infecting other cells
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Innate defenses
Virus
Viral nucleic acid
1 Virus
Internal defenses
New viruses
enters cell.
5 Antiviral
proteins block
viral
reproduction.
2 Interferon
genes switch on.
DNA
Nucleus
mRNA
4 Interferon
3 Cell produces
interferon
molecules.
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
binding
stimulates cell to
turn on genes for
antiviral proteins.
Figure 21.5, step 5
Second line of defense: Complement
“complete the action of antibody”
• 30 or so proteins synthesized mainly by the liver
• circulate in the blood in an inactive form and activated in
the presence of pathogen
• Proteins include C1 through C9, factors B, D, and P, and
regulatory proteins
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Second line of defense: Complement system functions
• Destruction of target cells membrane (MAC)
• Stimulation of inflammation – C3a stimulates mast cells and
basophils to secrete histamine
• Attraction of phagocytes
• Enhancement of phagocytosis –
• Phagocytes membrane carry receptors that can bind to the
complex of the complement proteins and antibodies.
• The binding results in much more efficient phagocytosis.
• The antibodies in such a complex are called opsonins and
the effect is called opsonization (enhanced attachment )
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Second line of defense: Natural killer (NK) cells
• Are a small, distinct group of large granular lymphocytes
• React nonspecifically and eliminate cancerous and virus-infected
cells
• Kill their target cells by releasing perforins and other cytolytic
chemicals
• Secrete potent chemicals that enhance the inflammatory response
• NK cells
• Recognize cell surface markers on foreign/abnormal cells
• Recognize variety of antigens (less selective)
• Immediate response when contact abnormal cells
• Destroy cells with foreign antigens
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Properties of specific immunity
• Specificity – activated by and responds to a specific
antigen
• Versatility – is ready to confront any antigen at any time
• Memory – “remembers” any antigen it has encountered
• Tolerance – responds to foreign substances but ignores
normal tissues
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Complete Antigens
• Substances that can mobilize the immune system and
provoke an immune response
• mostly large, complex molecules not normally found in
the body (nonself)
• Important properties of antigene:
• Immunogenicity – ability to stimulate proliferation
of specific lymphocytes and antibody production
• Reactivity – ability to react with products of
activated lymphocytes and the antibodies released in
response to them
• Complete antigens include foreign protein, nucleic acid,
some lipids, and large polysaccharides
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Haptens (Incomplete Antigens)
• Small molecules, such as peptides, nucleotides, and
many hormones, that are not immunogenic but are
reactive when attached to protein carriers
• If they link up with the body’s proteins, the adaptive
immune system may recognize them as foreign and
mount a harmful attack (allergy)
• Haptens are found in poison ivy, dander, some
detergents, and cosmetics
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The formation of an antigen-antibody complex
Carrier
molecule
Antibodies bind not to the entire
antigen, but to specific portions of
its exposed surface—regions
called antigenic determinant
sites.
Antibody
Antigen-antibody
complex
A complete antigen is an
antigen with at least two antigenic
determinant sites, one for each of
the antigen binding sites on an
antibody molecule.
Partial antigen
(hapten)
Antibody
Partial antigens, or haptens, do not
ordinarily cause B cell activation.
However, they may become attached to
carrier molecules, forming combinations
that can function as complete antigens.
The antibodies produced will attack both
the hapten and the carrier molecule. If
the carrier molecule is normally present
in the tissues, the antibodies may begin
attacking and destroying normal cells.
This is the basis for several drug
reactions, including allergies to
penicillin.
Figure 19.14 2
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Cells of the Adaptive Immune System
• Two types of lymphocytes
• B lymphocytes – oversee humoral immunity
• T lymphocytes – non-antibody-producing cells that
constitute the cell-mediated arm of immunity
• Antigen-presenting cells (APCs):
• Do not respond to specific antigens
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Lymphocytes can become immunocompetent
• Immature lymphocytes released from bone marrow are
identical
• During their development the lymphocyte:
• Must become able to recognize its one specific
antigen – become immunocompetent
• Must be relatively unresponsive to self so it will not
attack the body’s own cells – self tolerance
• Location of becoming immunocompetent is the key for a
lymphocyte to become B cell or a T cell
• B cells mature in the bone marrow
• T cells mature in the thymus
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Immunocompetent B or T cells
• It is genes, not antigens, that determine which foreign
substances our immune system will recognize and resist
• Become immunocompetent before they encounter
antigens they may later attack
• Immunocompetence - displaying a unique type of
receptor that responds to a specific antigen
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Immunocompetent B or T cells
• An immunocompetent cell divides rapidly to form a
clone of cells with identical receptors. All clones yet to
encounter an antigen are called the virgin/naive
lymphocyte pool.
• Are exported to secondary lymphoid tissue where
encounters with antigens occur
• Mature into fully functional antigen-activated cells upon
binding with their recognized antigen
• Clonal selection of B or T cells occurs when antigens
bind to their receptors, causing them to proliferate.
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Antigen-Presenting Cells (APCs)
• Major functions in immunity are:
• To engulf foreign particles
• To present fragments of antigens on their own surfaces, to be
recognized by T cells
• Major APCs are
• Dendritic cells (DCs),
• Dendritic cells (DC) are bone marrow-derived cells that are
specialized to take up, process and present antigen
• Dendritic cells are present in small quantities in tissues that
are in contact with the external environment, mainly the skin
(where they are often called Langerhans cells) and the inner
lining of the nose, lungs, stomach and the intestines.
• Macrophages that are found all over the body
• Activated B cells
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Antigen-Presenting Cells Display Foreign Proteins
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Figure 24-4 (4 of 4)
Importance of Cellular and humoral Responses
• Importance of Humoral Response (Soluble antibodies)
• The simplest ammunition of the immune response
• Interact in extracellular environments such as body secretions,
tissue fluid, blood, and lymph
• Importance of Cellular Response (T-cells)
• T cells recognize and respond only to processed fragments of
antigen displayed on the surface of body cells
• T cells are best suited for cell-to-cell interactions, and target:
• Cells infected with viruses, bacteria, or intracellular
parasites
• Abnormal or cancerous cells
• Cells of infused or transplanted foreign tissue
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Primary Response
(initial encounter
with antigen)
B lymphoblasts
Proliferation to
form a clone
Plasma
cells
Antigen
Antigen binding
to a receptor on a
specific B lymphocyte
(B lymphocytes with
non-complementary
receptors remain
inactive)
Memory
B cell
Secreted
antibody
molecules
Secondary Response
(can be years later)
Clone of cells
identical to
ancestral cells
Subsequent
challenge by
same antigen
Plasma
cells
Secreted
antibody
molecules
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Memory
B cells
Figure 21.10
Antibodies
• Also called immunoglobulins
• Plasma cells make over a billion types of antibodies
• makes the gamma globulin portion of blood proteins
• Are soluble proteins secreted by activated B cells and
plasma cells in response to an antigen
• Are capable of binding specifically with that antigen
• Antibodies themselves do not destroy antigen; they
inactivate and tag it for destruction
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Basic Antibody Structure
• Consists of four polypeptide chains linked together with
disulfide bonds
• Two identical heavy (H) chains and two identical light
(L) chains
• The four chains bound together form an antibody monomer
• Each chain has a variable (V) region at one end and a
constant (C) region at the other
• Variable (FAB) regions of the heavy and light chains
combine to form the antigen-binding site
• Constant (FC) region Determine the class of the
antibody (one of the 5 groups)
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Antibody Structure
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Classes of Antibodies
• IgD – monomer attached to the surface of B cells,
important in B cell activation
• IgM – pentamer released by plasma cells during the
primary immune response
• IgG – monomer that is the most abundant and diverse
antibody in primary and secondary response; crosses the
placenta and confers passive immunity
• IgA – dimer that helps prevent attachment of pathogens to
epithelial cell surfaces
• IgE – monomer that binds to mast cells and basophils,
causing histamine release when activated
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http://www.as.wvu.edu/~rbrundage/chapter12b/sld012.htm
Neutralization – by binding to specific sites on the antigen,
the antibody prevents its binding to cells
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Actions of antibodies – agglutination and precipitation
• Ab molecules have at least 2 binding sites
• Ag have many antigenic determinant sites
• When Ag are far apart Ab will bind with 2 binding sites to the same
antigen
• If Ag are close, Ab can bind to antigenic determinant sites of
different Ag.
• As a consequence, the Ab “tie” Ag molecules together. Such a
complex is called immune complex
• When the complexes are too big to be soluble they “sink” in a
process called precipitation
• When the target Ag are on the surface of the cell or virus the
formation of the large complex is called agglutination (example:
clumping of RBCs in incompatible blood transfusion)
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http://www.as.wvu.edu/~rbrundage/chapter12b/sld012.htm
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Complement Fixation and Activation
• Complement fixation:
• Main mechanism used against cellular antigens
• Antibodies bound to cells change shape and expose
complement binding sites
• This triggers complement fixation and cell lysis
• Complement activation:
• Enhances the inflammatory response
• Uses a positive feedback cycle to promote
phagocytosis
• Enlists more and more defensive elements
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Activation of complement (nonspecific reaction) – when
antibody bind to antigen, the Ab shape changes and that allows
the binding of the complement proteins (which pathway?)
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The prevention of bacterial and viral adhesion
• Covered by Ab, pathogens have reduced ability to attach to
body surfaces and penetrate.
Fig. 1: Bacterial
Adherence Via Pili
Fig. 1A: Blocking Bacterial
Adherence with Antibody
Molecules
http://www.cat.cc.md.us/courses/bio141/lecguide/unit3/humoral/abydefense/opsonization/opsonization.html
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Phagocytes membrane carry receptors that can bind to the complex of the
complement proteins and antibodies. The binding results in much more
efficient phagocytosis. The antibodies in such a complex are called
opsonins and the effect is called opsonization (enhanced attachment )
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Mechanisms of Antibody Action - summary
Adaptive defenses
Humoral immunity
Antigen
Antigen-antibody
complex
Antibody
Inactivates by
Neutralization
(masks dangerous
parts of bacterial
exotoxins; viruses)
Agglutination
(cell-bound antigens)
Enhances
Phagocytosis
Fixes and activates
Precipitation
(soluble antigens)
Enhances
Complement
Leads to
Inflammation
Cell lysis
Chemotaxis
Histamine
release
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Figure 21.15
Immunological Memory
• Primary response – the initial response to an antigen
• Cellular differentiation and proliferation, which occurs on the first
exposure to a specific antigen
• Lag period: 3 to 6 days after antigen challenge
• Peak levels of plasma antibody are achieved in 10 days
• Antibody levels then decline
• If the antigen is not present anymore, the antibody production
decrease. This reduction happens because:
• Plasma cells have short life span (few days)
• Suppressor T cells suppress plasma cells production
• IgM molecules are the first to appear during primary response. IgM
provide the immediate defense. This defense is limited because no
memory cells are being produced
• IgG – rise slow. Memory cells are formed
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Secondary antibody response
• Secondary immune response – re-exposure to the same antigen
• Sensitized memory cells respond within hours
• Antibody levels peak in 2 to 3 days at much higher levels than in
the primary response
• Antibodies bind with greater affinity, and their levels in the blood
can remain high for weeks to months
• Memory B cells can leave for 20 years or longer
• When a second exposure to antigen occur, memory B cells
differentiate into plasma cells
• This response is immediate because memory B cells are activated by
relatively low levels of antigen
• The antibody titer rises rapidly and to higher levels than during
primary response
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The Primary and Secondary Immune Responses
Figure 22.22
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Humoral
immunity
Active
Passive
Naturally
acquired
Artificially
acquired
Naturally
acquired
Artificially
acquired
Infection;
contact
with
pathogen
Vaccine;
dead or
attenuated
pathogens
Antibodies
pass from
mother to
fetus via
placenta;
or to infant
in her milk
Injection of
immune
serum
(gamma
globulin)
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Figure 21.13
Antigen Recognition and MHC Restriction
• Immunocompetent T cells are activated when the
variable regions of their surface receptors bind to a
recognized antigen
• T cells must recognize:
• Nonself (the antigen)
• Self (a MHC protein of a body cell)
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Specific T-cells roles: Helper T Cells (TH)
• Regulatory cells
• Once primed by APC presentation of antigen, they:
• Chemically or directly stimulate proliferation of
other T cells (using protein mediators called
lymphokines)
• In the absence of lymphokines the immune system is
almost paralyzed
• Without TH, there is no immune response
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Lymphokines functions
• Promote the growth and proliferation of other T cells
(cytotoxic and suppressor)
• Stimulate B-cells growth and differentiation to plasma
cells
• Amplify innate defense mechanisms
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Specific T-cells roles: Cytotoxic T Cell (Tc)
• TC cells, or killer T cells, are the only T cells that can
directly attack and kill other cells
• They circulate throughout the body in search of body cells
that display the antigen to which they have been sensitized
• Their targets include:
• Virus-infected cells
• Cells with intracellular bacteria or parasites
• Cancer cells
• Foreign cells from blood transfusions or transplants
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Mechanisms of Tc Action
• Bind to the target cell and release perforin into its
membrane
• In the presence of Ca2+ perforin causes cell lysis
by creating transmembrane pores
• Secreting lymphotoxin, which fragments the target cell’s
DNA
• Secreting
gamma
interferon,
phagocytosis by macrophages
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which
stimulates
Antigen Recognition and the Activation of Cytotoxic T Cells
Figure 22.17
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Other T Cells
• Suppressor T cells (TS) – regulatory cells that release
cytokines, which suppress the activity of both T cells and
B cells
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Self-Antigens: MHC Proteins
• Major histocompatibility complex - MHC proteins,
mark a cell as self
• The two classes of MHC proteins are:
• Class I MHC proteins – found on virtually all body
cells
• Class II MHC proteins – found on certain cells in
the immune response
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MHC classes – class I
• Class I – found on all nucleated cells (“hey, I’m an abnormal
cell – please kill me”)
• “Sign” infected, sick or abnormal cells that need to be
destroyed by the T-cells
• When type I are forming they “pick up” peptides from the
cytoplasm and carry them to the cell surface
• If the peptides are normal (healthy cell) the T-cells will
ignore them
• If the cytoplasm contain abnormal peptides or viral
proteins, T-cells will be activated. This activation will
lead to the cell destruction
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MHC classes – class I
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MHC classes – class II
• Class II MHC proteins are found only on mature B cells,
some T cells, and antigen-presenting cells (“Hey, this
antigen is dangerous – get rid of it”)
• Class II are found on cells that the body does not need to
destroy – it is only a mean to present non-self material
• Phagocytes cells engulf and break down pathogens
• A phagosome containing pathogens (with exogenous
antigens) merges with a lysosome
• This antigen processing creates fragments that are bound
to type II MHC and inserted into the cell membrane
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MHC classes – class II
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Cell-Mediated Immune Response
• Two major populations of T cells mediate cellular immunity:
• CD4 cells (T4 cells) are primarily helper T cells (TH)
• CD8 cells (T8 cells) are cytotoxic T cells (TC) that
destroy cells with foreign antigens
• MHC restriction – TH and TC bind to different classes of
MHC proteins
• TH / CD4 cells bind to antigen linked to class II MHC
proteins
• TC / CD8 cells are activated by antigen fragments presented
by class I MHC proteins
Copyright © 2010 Pearson Education, Inc.
Copyright © 2010 Pearson Education, Inc.
Presentation of Antigen to T cells
Copyright © 2010 Pearson Education, Inc.
A Summary of the Pathways of T Cell Activation
Figure 22.19
Copyright © 2010 Pearson Education, Inc.