Download The Immune System - Body Defenses

BIO2305
Immune System - Body Defenses
Body Defenses – 1st Line of Defense
Reconnaissance, Recognition, and Response
Must defend from the many dangerous pathogens it may encounter in the environment
– Detect invader/foreign cells
– Communicate alarm & recruit immune cells
– Suppress or destroy invader
Two major kinds of defense have evolved that counter these threats
– Innate immunity and acquired immunity
Innate Immunity
• Innate immunity provides broad defenses against infection
• Present before any exposure to pathogens and is effective from the time of birth
• Involves nonspecific responses to pathogens
• A pathogen that successfully breaks through an animal’s external defenses encounters several
innate cellular and chemical mechanisms that impede its attack on the body
• Non-selective and no lag time – immediate response, no previous exposure required
• Protects against infections, toxins
• Works with specific (acquired) immune response
Acquired (Adaptive) Immune Response
- Depends on B and T lymphocytes
- Specific immune response directed attack against pathogens (antigen)
- Lag time
- Previous Antigen exposure required
- Protects against pathogens and cancer cells
- Types
- Antibody-mediated: B cells
- Cell-mediated: T cells
Types of Immunity
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Body Defenses
INNATE IMMUNITY
Rapid responses to a
broad range of microbes
External defenses
Skin
Internal defenses
Phagocytic cells
Mucous membranes
Antimicrobial proteins
Secretions
Inflammatory response
Invading
microbes
(pathogens)
ACQUIRED IMMUNITY
Slower responses to
specific microbes
Natural killer cells
Humoral response
(antibodies)
Cell-mediated response
(cytotoxic
lymphocytes)
Innate Immunity
• Physical barriers, secretion, chemical toxins
• Phagocytosis - macrophages neutrophils engulf and digest recognized "foreign" cells –
molecules
• Inflammatory response - localized tissue response to injury producing swelling, redness, heat,
pain
• Natural Killer cells – special class of lymphocyte-like cells that destroy virus infected cells and
cancer cells
• Complements system activated proteins that destroy pathogen plasma membranes and
enhance phagocytosis, inflamation
• Interferon - proteins that non-specifically defend against viral infection
Innate Immunity / External Defenses
 Physical barriers prevent entry of microorganisms & viruses
1. Epidermis - provides a physical barrier, periodic shedding removes microbes
2. Mucous membranes and mucus - traps microbes and foreign particles
3. Hair - within the nose filters air containing microbes, dust, pollutants
4. Cilia - lines the upper respiratory tract traps and propels inhaled debris to throat
5. Lacrimal apparatus - produces tears that cleanse the eye
6. Saliva - dilutes the number of microorganisms and washes the teeth and mouth
7. Urine - flush microbes out of the urethra
8. Defecation and vomiting - expel microorganisms.
 Chemical factors
1. Skin acidity - inhibit bacterial growth b/w 3 & 5
2. Sebum -unsaturated fatty acids provide a protective film and inhibit growth, toxic to microbes
3. Lysozyme- found in perspiration, tears, saliva can breakdown the cell wall of certain bacterial
4. Hyaluronic acid - gelatinous substance that slows the spread of noxious agents
5. Gastric Juice - strong acid that destroys ingested microbes and most toxins
•
In the trachea, ciliated epithelial cells sweep mucus
and any entrapped microbes upward, preventing
the microbes from entering the lungs
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Immune System Functions
1. Scavenge dead, dying body cells
2. Destroy abnormal (cancerous)
3. Protect from pathogens & foreign molecules: parasites, bacteria, viruses
Steps in Immune defense
 Detect invader/foreign cells, communicate alarm & recruit immune cells, suppress or destroy
invader
Innate Immunity – Phagocytosis
• Scavenge dead, dying body cells, remove cellular debris
• Engulf and digest recognized "foreign" cells
• Destroy abnormal (cancerous)
• Protect from pathogens & foreign molecules: parasites, bacteria, viruses
– Monocyte - macrophage system – free and fixed
– Margination – stick to the inner endothelial lining of capillaries of affected tissue
– Move by diapedesis – move thru capillary walls
– Microphages – Neutrophils and eosinophils
– Exhibit chemotaxis
Phagocytes release chemical mediators
• Kinins - stimulate complement system (plasma proteins), chemotaxins, pain
• Clotting factors – walling off invasion
• Lysosomal enzymes – destroy invaders
Neutrophils
Fastest response of all WBC to bacteria and parasites
Direct actions against bacteria
- Release lysozymes which destroy/digest bacteria
- Release defensive proteins that act like antibiotics
- Release strong oxidants (bleach-like, strong chemicals) that destroy bacteria
Eosinophils
- Leave capillaries to enter tissue fluid
- Attack parasitic worms
- Phagocytize antibody-antigen complexes
Monocytes
- Take longer to get to site of infection, but arrive in larger numbers
- Become free (roaming) macrophages, once they leave the capillaries
- Destroy microbes and clean up dead tissue following an infection
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Phagocytic Cells
 Phagocytes attach to their prey via surface receptors and engulf them, forming a vacuole that fuses
with a lysosome
1
Pseudopodia
surround
microbes.
Microbe
s
2 Microbes
areengulfed
into cell.
MACROPHAG
E
3
Vacuole
containing
microbes
forms.
Vacuol
e
Lysosom
e
containin
g
enzymes
4 Vacuole
and lysosome
fuse.
5 Toxic
compounds
and lysosomal
enzymes
destroy microbes.
6Microbial
debris is
released by
exocytosis.
Phagocytosis Mechanisms
• Chemotaxis
• Attraction to certain chemical mediators
• Released at the site of damage
• Chemotaxins induce phagocytes to injury
• Opsonization
• Identify (mark) pathogen
• Coated with chemical mediators
• Most important opsonins
• Toll-like receptors (TLR’s)
• Phagocytic cells studded with plasma membrane receptor proteins
• Bind with pathogen markers
• Recognition - Allow phagocytes to “see” and distinguish from self-cells
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Inflammatory Response
• Inflammation – histamine release from mast cells and other chemicals released from injured
cells promote changes in blood vessels
• Changes allow more fluid, phagocytes, and antimicrobial proteins to enter tissues
• Effects of inflammation include
– Mobilization of local, regional, and systemic defenses
– Slow the spread of pathogens
– Temporary repair of injury
•
•
Macrophages, mast cells release histamine
– Localized vasodilation
– Capillary permeability - increased gaps in capillaries bring more WBC's & plasma
proteins
– Swelling, redness, heat and pain are incidental
Injured cells and phagocytes release cytokines (chemical signals)
– Kinins - stimulate complement system (plasma proteins)
– Chemotaxins – attract more phagocytes
– Clotting factors – walling off invasion
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Blood clot
Pin
Pathogen
Macrophage
Chemical signals
Phagocytic cells
Capillary
Blood
clotting
elements
Phagocytosis
Red blood cell
Chemical signals released
1 by activated macrophages
and mast cells at the injury
site cause nearby capillaries
to widen and become more
permeable.
2 Fluid, antimicrobial proteins,
and clotting elements move
from the blood to the site.
Clotting begins.
3 Chemokines released by various 4 Neutrophils and macrophages
phagocytose pathogens and
kinds of cells attract more
cell debris at the site, and the
phagocytic cells from the blood
tissue heals.
to the injury site.
Natural Killer Cells
- Patrol the body and attack virus-infected body cells and cancer cells
- Recognize cell surface markers on foreign cells
- Destroy cells with foreign antigens
- Rotation of the Golgi toward the target cell and production of perforins
- Release of perforins by exocytosis
- Interaction of perforins causing cell lysis
How Natural Killer Cells Kill Cellular Targets
Antimicrobial Proteins
• Proteins function in innate defense by attacking microbes directly or impeding their
reproduction
– Complement System - About 30 proteins involved in the lysis of invading cells and helps
trigger inflammation
– Interferons – small proteins provide innate defense against viruses and help activate
macrophages
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Complement System
• System of inactive proteins produced by liver circulating in blood and on cell membranes
• Cascade of plasma complement proteins (C) activated by antibodies or antigens causing
cascade of chemical reactions
• Direct effect is lysis of microorganisms by destroying target cell membranes
• Indirect effects include:
– Chemotaxis
– Opsonization
– Inflammation: recruit phagocytes, B & T lymphocytes
Compliment Activation
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Innate Cytokines - Interferons
• Small antiviral proteins released by lymphocytes, macrophages, virally infected cells
• 3 Major types of interferons are:
– Alpha– produced by leukocytes and attract/stimulate NK cells
– Beta– secreted by fibroblasts causing slow inflammation
– Gamma – secreted by T cells and NK cells stimulate macrophage activity
• Type I interferons – Alpha and Beta
– Induced during many virus infections
• IFN- a: Mainly by leukocytes
• IFN- b: Mainly by fibroblast cells
– Binds to membranes of adjacent, uninfected cells
– Triggers production of proteins that interfere with viral replication
– Enhances macrophage, natural killer, and cytotoxic T cell & B cell activity
– Slows cell division and suppresses tumor growth
• Type II Interferon - gamma
– Activates macrophages and other immune cells
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Integrated Defense
Bacteria enter extracellular
fluid from outside
EXTERNAL ENVIRONMENT
SKIN OR MUCOUS MEMBRANE
lyses
ECF
coat
Opsonins
ingest and
disable
act as
Bacteria
Membrane
attack complex
activate
make
Complement
proteins
activate
Mast cells
are
Acute phase
proteins
Phagocytes
secrete
Chemotaxins
Antibodies
Histamine
increases
permeability
act as
CAPILLARY
Plasma proteins
Circulating leukocytes
attract
Acquired Immunity
• In acquired immunity, lymphocytes provide specific defenses against infection
• Involves
– Cell mediated immunity: T cells
– Antibody mediated immunity: B cells
• Depends on B and T lymphocytes - specific immune response directed attack against
pathogens (antigen)
• Lag time ~ two weeks, previous Antigen exposure required
• Protects against pathogens and cancer cells
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Acquired Immunity
• Antigen triggers an immune response
• Activates T cells and B cells
– T cells are activated after phagocytes exposed to antigen
• T cells attack the antigen and stimulate B cells
• Activated B cells mature and produce antibody
• Antibody attacks antigen
Properties of Acquired 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
Lymphatic System
• Primary lymphatic organs – Bone marrow and Thymus
– Lymphocytes mature into functional cells (red bone marrow B cells and thymus T cells)
– Bone marrow – origin of blood cells
– Thymus – site of maturing T Lymphocytes
• Secondary lymphatic organs - lymph nodes, spleen
– Site of immune response – lymph nodes
– Lymph nodes – Exchange Lymphocyte w/ lymph (remove, store, produce, add)
• Resident macrophages remove microbes and debris from lymph
• Lymphocytes produce antibodies and sensitized T cells released in lymph
– Spleen – Exchange Lymphocytes with blood, residents produce antibodies and
sensitized T cells released in blood
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Lymphocytes
• B cells originate and mature in bone marrow
• T cells originate in bone marrow, migrate then mature in thymus
Bone marrow
Thymus
Lymphoid
stem cell
B cell
T cell
Blood, lymph, and lymphoid tissues
(lymph nodes, spleen, and others)
Antigens
• An antigen is any foreign molecule that is specifically recognized by lymphocytes and elicits a
response from them
• A lymphocyte actually recognizes and binds to just a small, accessible portion of the antigen
called an epitope or antigenic determinant
– Antigenic determinants - Specific regions of a given antigen recognized by a lymphocyte
– Antigenic receptors -Surface of lymphocyte that combines with antigenic determinant
Antigenbinding
sites
Epitopes
(antigenic
determinants)
Antigen
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Antigen Recognition by Lymphocytes
• A single B cell or T cell has about 100,000 identical antigen receptors
• All antigen receptors on a single cell recognize the same epitope
Disulfide
bridge
V
V
Variable regions
C
C
V
V
Light
chain
Antigenbinding
site
Antigenbinding site
Antigenbinding
site
C
C
Constant regions
V
V
C
C
Transmembrane
region
Heavy chains
Plasma
membrane
 chain
 chain
Disulfide bridge
B cell
Cytoplasm of B cell
A B cell receptor consists of two identical heavy chains
and two identical light chains linked by several disulfide
bridges.
Cytoplasm of T cell
T cell
A T cell receptor consists of one  chain
and one  chain linked by a disulfide
bridge.
Cell-Mediated Immunity – T Cells
• Antigens that stimulate this response are mainly intracellular (cell to cell).
• Requires constant presence of antigen to remain effective
• Involves numerous cytokines, over 100 have been identified
• Stimulate and/or regulate immune responses
– Interleukins: Communication between WBCs
– Interferons: Protect against viral infections
– Chemotaxins: Attract WBCs to infected areas
Lymphocyte Communication
• Over 18 different types of interleukins are known; designated IL-1, IL-2…IL-18, etc.
• IL-1 and IL-2 are primarily responsible for activating T and B lymphocytes, with IL-2 being a
stimulant of T- and B-cell growth and maturation
• IL-1, along with IL-6, is also a mediator of inflammation.
• IL-4 often leads to an increase in antibody secretion by B lymphocytes
• IL-12 causes a greater number of the leukocytes cytotoxic T cells and natural killer cells to be
made
• The set of interleukins produced by the presence of a specific infectious agent determines
which cells will respond to the infection
Major types of T cells
• Cytotoxic T cells – attack foreign cells
• Helper T cells - activate other T cells and B cells
• Suppressor T cells– inhibit the activation of T and B cells
• Memory T cells – function during a second exposure to antigen
• T cell membranes contain CD markers
– CD3 markers present on all T cells
– CD8 markers on cytotoxic and suppressor T cells
– CD4 markers on helper T cells
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Cell-Mediated Immunity – T Cell activation
• T cells are activated when they detect and bind to small fragments of antigens that are
combined with to cell-surface glycoproteins called major histocompatability complex (MHC)
molecules
• Lymphocytes respond to antigens bound to either class I or class II MHC proteins depending
on the source of the MHC molecule and antigen presenting cell
• Class I MHC molecules are displayed on the surface of infected nucleated cells, resulting in
destruction of cells
• Class II MHC molecules are displayed on the surface of phagocytes (antigen-presenting cells),
resulting in activation of immune cells
Antigen Presenting Cells
• Macrophages & Dendritic Cells engulf foreign antigens by phagocytosis, proteins broken down
into peptides
• Peptides go to ER and Golgi where they are attached to new MHC self antigen molecules
• New self antigen and its antigen fragment are added to the cell membrane and presented to
lymphocytes
• T Cells Only Recognize Antigen Associated with MHC Molecules on Cell Surfaces
Class 1 MHC Molecules
• Infected cells produce class I MHC molecules which bind to antigen fragments and then are
transported to the cell surface in a process called antigen presentation
• Binds and activates with cytotoxic T cell receptor
• Cytotoxic T cell response
– Clonal production of cytotoxic T cells and memory cells
– Destruction of virus-infected cells, tumor cells, and tissue transplants
Released
cytotoxic
T cell
Cytotoxic T cell
Perforin
Cancer
cell
Granzymes
TCR
CD8
Class I MHC
molecule
Target
cell
Pore
Peptide
antigen
Apoptotic
target cell
Cytotoxic
T cell
Cytotoxic T (TC) Cells – Destroy Target Cells CD8
• Killer Ts or CD8
• Recognize and destroy host cells that are infected with viruses or bacteria, cancer cells,
transplanted tissue
• Release protein called perforin which forms a pore in target cell, causing lysis of infected cells.
• Produce cytokines, which promote phagocytosis and inflammation
• Undergo apoptosis when stimulating antigen is gone.
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Class II MHC molecules
• Produced by dendritic cells, macrophages, and B cells
• Macrophages & dendritic cells phagocytize antigens, proteins broken down into antigen
fragments (peptides) and combined with Class II MHC molecules
• Binds and activates Helper T cells
– Clonal production of Helper T cells
– Activation of Cytotoxic T cells
– Activation of B cells
Peptide antigen
Dendritic
cell
Class II MHC
molecule
Cytotoxic T cell
Helper T cell
Bacterium
TCR
CD4
Dendritic
cell
Cytokines B cell
Cell-mediated
immunity
(attack on
infected cells)
Humoral
immunity
(secretion of
antibodies by
plasma cells)
T Helper (TH) Cells – CD4
• T Helper (TH) Cells: main role in immune response
• Recognize antigen on the surface of antigen presenting cells
• Secrete Interleukin II (T-cell growth factor), interferon and cytokines which stimulate
lymphocyte activity
• Production and activation of Cytotoxic T cells and more Helper T cells
• Stimulate B cells to produce antibodies
14
T Cell Overview
Memory T-Cells
• Can survive a long time and give lifelong immunity from infection
• Can stimulate memory B-cells to produce antibodies
• Can trigger production of killer T cells
• Thymosin - hormone important in T cell lineage, enhances capabilities of existing T cells and
the proliferation of new T cells in lymphoid tissues - decreases after age 30-40
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Proliferation of Lymphocytes
Cell-mediated immune response
Humoral immune response
First exposure to antigen
Intact antigens
Antigens engulfed and
displayed by dendritic cells
Antigens displayed
by infected cells
Activate
Activate
Activate
B cells
Gives rise to
Plasma
cells
Memory
B cells
Secreted
cytokines
activate
Helper
T cell
Gives rise to
Active and
memory
helper
T cells
Cytotoxic
T cell
Gives rise to
Memory
cytotoxic
T cells
Active
cytotoxic
T cells
Defend against infected cells, cancer
cells, and transplanted tissues
Secrete antibodies that defend against
pathogens and toxins in extracellular fluid
Antibody-Mediated (Humoral) Immunity
• Involves production of antibodies against foreign antigens
• Antibodies are produced B cells
• B cells that are stimulated will actively secrete antibodies and are called plasma cells
• Antibodies (immunoglobulins, Ig) are found in extracellular fluids (blood plasma, lymph,
mucus, etc.) and the surface of B cells.
• Defend against bacteria, bacterial toxins, and viruses that circulate freely in body fluids, before
they enter cells
• Also cause certain reactions against transplanted tissue
• 1000s of different B cells, each recognizes a different antigen on the surface of a macrophage.
• Each antigen stimulates production of a single specific antibody that the B cells (along with T
cells) come in contact with
• They are stimulated (by TH cells) to produce many clones, plasma cells, which make
antibodies.
• Memory B cells – secondary response = faster, more sensitive
Macrophage
Bacterium
Peptide
antigen
B cell
Class II MHC
molecule
TCR
Secreted antibody
molecules
Endoplasmic
reticulum of
plasma cell
Clone of plasma cells
CD4
+
Cytokines
Helper T cell
Activated
helper T cell
Clone of memory
B cells
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Antibody Structure
• Antibodies or Immunoglobulins (Ig)
– Classes: IgG, IgM, IgA, IgE, IgD
– Structure
• Variable region - combines with anitgenic determinant of antigen
• Constant region - responsible for other binding activities
Antigen
binding
site
Light
chain
Antigenbinding site
V
V
Disulfide
V
bridge
V
Variable regions
C
C
C C
Constant regions
Heavy chains
Antibodies
• (Immunoglobulins, Ig) are proteins that recognize specific antigens and bind to them.
• They are found in extracellular fluids (blood plasma, lymph, mucus, etc.) and the surface of B
cells
• Defense against bacteria, bacterial toxins, and viruses that circulate freely in body fluids, before
they enter cells.
• Also cause certain reactions against transplanted tissue.
• Antigenic determinants - specific regions of a given antigen recognized by a lymphocyte
• Antigenic receptors are found on surface of lymphocyte that combines with antigenic
determinant to form Antigen-Antibody Complex
• Antibodies affinity: A measure of binding strength.
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Consequences of Antigen- Antibody Binding
– Agglutination - antibodies cause antigens (microbes) to clump together
– Opsonization and Phagocytosis
– Activates Complement System / Inflammatory Response
– Neutralization
– Antibody dependent NK / eosinophil cell response
Antigen-Antibody Complex on B Cell
• Activate B lymphocyte production of:
– Memory cells for secondary immune response to that antigen
– Plasma cells that secrete antibodies
6 Activates
complement
1 Activates B
lymphocytes
Antigen binds
to antibody
5 Triggers mast cell
degranulation
Antigen
binding
site
Antibody
Memory
cells
Plasma
cells
Secrete
antibodies
NK cell or eosinophil
4 Activates antibodydependent cellular
activity
3 Causes antigen clumping
and inactivation of
bacterial toxins
Bacterial
toxins
2 Acts as
opsonins
Enhanced
phagocytosis
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Immunoglobulin Classes
IgG
 Percentage serum antibodies: 80%,
 location: Blood, lymph, intestine Only lg that crosses placenta, thus conferring passive immunity
on fetus
 Promotes opsonization, neutralization, and agglutination of antigens, protects fetus and newborn
 Enhances phagocytosis, neutralizes toxins and viruses, protects fetus and newborn.
IgG
(monomer)
IgM
• Percentage serum antibodies: 5-10%
• Location: Blood, lymph, B cell surface (monomer)
• First antibodies produced during an infection. Effective against microbes, complement activation
and agglutinating antigens
IgM
(pentamer)
J chain
IgA
• Percentage serum antibodies: 10-15%
• Location: Secretions (tears, saliva, intestine, breast milk), blood and lymph
• Provides localized defense of mucous membranes by agglutination and neutralization of antigens
• Localized protection of mucosal surfaces. Presence in breast milk confers passive immunity on
nursing infant
IgA
(dimer)
J chain
Secretory
component
IgD
• Percentage serum antibodies: 0.2%
• Location: Found primarily on surface of naive B cells that have not been exposed to antigens
• Acts as antigen receptor in antigen-stimulated proliferation and differentiation of B cells (clonal
selection)
IgD
(monomer)
Transmembrane
region
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IgE
• Percentage serum antibodies: 0.002%
• Location: Bound to mast cells and basophils throughout body
• Triggers release of histamine and other chemicals that cause allergic reactions
IgE
(monomer)
B Cell Antibody Production
- B cells develop from stem cells in the bone marrow of adults (liver of fetuses).
- After maturation B cells migrate to lymphoid organs (lymph node or spleen).
- Clonal Selection: When a B cell encounters an antigen it recognizes, it is stimulated and
divides into many clones called plasma cells, which actively secrete antibodies.
- Each B cell produces antibodies that will recognize only one antigenic determinant.
B Cell Sensitization And Activation
• Sensitization – the binding of antigens to the B cell membrane antibodies
• Helper T cells present the same antigen to stimulate B cell
• Stimulated B cells divide into many clones called plasma cells, which actively secrete
antibodies
• Each B cell produces antibodies that will recognize only one antigenic determinant
• Active B cells also differentiate into Memory B Cells
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Immunological Memory
• Primary Response:
– After initial exposure to antigen, no antibodies are found in serum for several days. A
gradual increase number of Abs, first of IgM and then of IgG is observed.
– Most B cells become plasma cells, but some B cells become long living memory cells.
Gradual decline of antibodies follows.
• Secondary Response - Subsequent exposure to the same antigen displays a faster/more intense
response due to the existence of memory cells, which rapidly produce plasma cells upon
antigen stimulation
Clonal Selection
– Clonal Selection: B cells (and T cells) that encounter stimulating antigen will proliferate into a
large group of cells.
– Why don’t we produce antibodies against our own antigens? We have developed tolerance to
them.
– Tolerance: To prevent the immune system from responding to self-antigens
– Clonal Deletion: B and T cells that react against self antigens are normally destroyed
during fetal development
– Preventing activation of lymphocytes – activate suppressor T cells, control the immune
system when the antigen / pathogen has been destroyed
Apoptosis
– Programmed cell death (“Falling away”).
– Human body makes 100 million lymphocytes every day. If an equivalent number doesn’t die,
will develop leukemia.
– B cells that do not encounter stimulating antigen will self-destruct and send signals to
phagocytes to dispose of their remains.
– Many virus infected cells will undergo apoptosis, to help prevent spread of the infection.
Autoimmune Diseases: Failure of “Self-Tolerance”
• Some diabetes mellitus – attack - cells
• Multiple sclerosis – attack on myelin nerve sheath
• Rheumatoid arthritis – attack joint cartilage
• Myasthenia gravis – ACh-receptors at endplate attacked
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Allergic Response: Inflammation Reaction to Non-pathogen
- First exposure: sensitization and activation clone B cells that form antibodies and memory cells
- Re-exposure: many antibodies produced, activated Ts intensify inflammatory response
Summary
• Body defends itself with barriers, chemicals & immune responses
• WBCs and relatives conduct direct cellular attack: phagocytosis, activated NK & cytotoxic T
cells and produce attack proteins (i.e. antibodies, complement, & membrane attack complex)
• Cytokines, communicate cell activation, recruitment, swelling, pain, & fever in the
inflammation response
• Defense against bacteria is mostly innate while viral defense relies more on acquired immune
responses
• Autoimmune diseases are a failure of self-tolerance
Hemagglutination
• Agglutination of red blood cells used to determine ABO blood types and to detect influenza and
measles viruses
22
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