Download Defense against the dark arts

Defense against the dark arts
Section 1: Lymphatic System Anatomy
• Lymphatic system includes cells, tissues, and
organs responsible for defending the body
against:
– Environmental hazards (such as various pathogens)
– Internal threats (such as cancer cells)
• Lymphatics
– Network of lymphatic vessels
• Contains lymphocytes surrounded by lymph
similar to interstitial fluid)
(fluid
– Also includes array of lymphoid organs and tissues
Section 1: Lymphatic System
Anatomy
• Lymphocytes (primary cells of lymphatic
system)
– Respond to:
• Invading pathogens (such as bacteria and viruses)
• Abnormal body cells (such as virus-infected or cancer
cells)
• Foreign proteins (such as bacterial toxins)
– Mostly produced in lymphoid organs and tissues but
also in red bone marrow
Lymph
Lymphocyte
The components of the lymphatic system
Lymphatic Vessels and
Lymph Nodes
Cervical lymph nodes
Thoracic duct
Right lymphatic duct
Axillary lymph nodes
Lymphatics of mammary gland
Lymphoid Tissues
and Organs
Tonsil
Thymus
Cisterna chyli
Lymphatics of upper limb
Lumbar lymph nodes
Pelvic lymph nodes
Spleen
Mucosa-associated
lymphoid tissue
(MALT) in digestive,
respiratory, urinary,
and reproductive
tracts
Appendix
Inguinal lymph nodes
Lymphatics of lower limb
Figure 19 Section 1
Module 19.1: Lymphatic capillaries
• Lymphatic vessels
– Carry lymph from peripheral tissues to venous
system
– Network begins with lymphatic capillaries
(smallest vessels)
• Collect interstitial fluid (then called lymph) and
transport it to larger lymphatic vessels
– Larger vessels are similar in structure to veins
• Have valves
The flow of interstitial fluid into lymphatic capillaries, where it is called lymph
Arteriole
Smooth muscle
Endothelial cells
Lymphatic capillary
Blood capillaries
Loose connective
tissue
Venule
Interstitial
fluid
Lymph
flow
Figure 19.1
1
Artery
Vein
Lymphatic
vessel
The flow of lymph from lymphatic capillaries to
larger lymphatic vessels on the way to the venous system
Vein
Artery
Lymphatic vessel
To larger lymphatic vessels
that deliver lymph to the venous system
Lymphatic valve
From lymphatic
capillaries
Lymphatic valve
Lymphatic vessel
Valve in lymphatic vessel
LM x 65
Figure 19.1
3 – 4
Module 19.1: Lymphatic
capillaries
• Lymphatic capillaries
– Present in almost every tissue, alongside
cardiovascular capillaries
• Differ from blood capillaries
1.
2.
3.
4.
5.
Originate as pockets rather than continuous tubes
Have larger diameters
Have thinner walls
» Basal lamina is incomplete or absent
Typically have a flattened or irregular outline in sectional
view
Endothelial cells overlap to form one-way valves
» Collect fluids as well as larger solutes
The structure of lymphatic capillaries
Lymphocyte
Loose
connective
tissue
Incomplete or absent
basal lamina
Lymph
flow
To larger
lymphatics
Overlapping
endothelial cells
Interstitial
fluid
Interstitial
fluid
Loose
connective
tissue
Lymphatic
capillary
Blood
capillary
Sectional view
Figure 19.1
2
Module 19.1 Review
a. What is the function of
lymphatic vessels?
b. What structure prevents
the backflow of lymph in
some lymphatic vessels?
c. What is the function of
overlapping endothelial
cells in lymphatic
capillaries?
Module 19.2: Lymphatic vessels
• Lymphatic vessel location
– Superficial lymphatics
•
•
•
Subcutaneous layer deep to skin
Areolar tissues of mucous membranes (digestive,
respiratory, urinary, and reproductive tracts)
Areolar tissues of serous membranes (pleural,
pericardial, and peritoneal cavities)
– Deep lymphatics
•
Accommodate deep arteries and veins supplying
skeletal muscles and other torso organs
Some characteristics of superficial and deep lymphatics
Lymphatic Vessels
Superficial Lymphatics
Deep Lymphatics
Are located in the subcutaneous layer deep to the skin;
in the areolar tissues of the mucous membranes lining
the digestive, respiratory, urinary, and reproductive
tracts; and in the areolar tissues of the serous
membranes lining the pleural, pericardial, and
peritoneal cavities
Accompany deep arteries and veins
supplying skeletal muscles and other
organs of the neck, limbs, and trunk,
and the walls of visceral organs
Superficial inguinal
lymph nodes and
lymphatic vessels
Deep inguinal
lymph nodes and
lymphatic vessels
Figure 19.2
1
Module 19.2: Lymphatic vessels
• Large lymphatic vessels
– Lymphatic trunks (drain lymph from large body
regions)
•
•
•
•
•
Jugular trunks
Subclavian trunks
Bronchomediastinal trunks
Lumbar trunks
Intestinal trunk
– Cisterna chyli
•
Expanded chamber receiving lymph from lumbar trunks
and intestinal trunk
Module 19.2: Lymphatic
vessels
• Large lymphatic vessels (continued)
– Lymphatic ducts (empty into subclavian veins)
•
Right lymphatic duct
–
•
Drains lymph from right arm, right upper torso, right head
and neck
Thoracic duct
–
Drains lymph from rest of body
» Left arm, lower limbs, lower torso, upper left torso,
left head and neck
Areas of the body drained by the right lymphatic
and thoracic ducts
Drainage of right
lymphatic duct
Drainage of
thoracic duct
Figure 19.2
2
The relationship between the right lymphatic and thoracic ducts and the venous system
Right internal
jugular vein
Right Lymphatic Duct
Is formed by the merging of the
trunks labeled below
Brachiocephalic
veins
Left internal
jugular vein
Thoracic Duct
Collects lymph from the trunks
labeled below
Right jugular trunk
Left jugular trunk
Right subclavian trunk
Left subclavian trunk
Right lymphatic duct entering
right subclavian vein
Thoracic duct entering
left subclavian vein
Left bronchomediastinal trunk
Right bronchomediastinal trunk
Superior vena cava (cut)
Rib (cut)
Thoracic duct
Azygos vein
Thoracic
lymph nodes
Parietal
pleura (cut)
Diaphragm
Intestinal trunk
Interior vena cava (cut)
Cisterna chyli
Right lumbar trunk
Left lumbar trunk
Figure 19.2
3
Module 19.2: Lymphatic vessels
•
Lymphedema
–
Blockage of lymphatic
drainage
Interstitial fluids
accumulate and affected
area swells
Most often seen in limbs
Can become permanent
and lead to infection
–
–
–
•
Interstitial fluid is
stagnant and pathogens
accumulate
Module 19.2 Review
a. Name the two large
lymphatic vessels into
which the lymphatic
trunks empty.
b. Explain lymphedema.
Module 19.3:
Lymphocytes
• Lymphocytes
– Account for 20%–30% of circulating leukocytes
•
•
Most lymphocytes are out in lymphatic tissues
Three classes circulate in blood
1.
2.
3.
T cells (80% of circulating lymphocytes)
» Cell-mediated immunity
B cells (10%–15% of circulating lymphocytes)
» Antibody-mediated immunity
NK cells (5%–10% of circulating lymphocytes)
» Immunological surveillance
Module 19.3: Lymphocytes
• All lymphocytes are sensitive to specific
chemicals (antigens)
– Antigens can be:
•
•
•
Pathogens
Parts or products of pathogens
Other foreign compounds
– Are usually proteins but can be other common
organic molecules as well
– Stimulate an immune response that leads to
destruction of target compound or organism
Module 19.3: Lymphocytes
•
Lymphocyte classes
–
T cells (three major
categories)
1.
Cytotoxic T cells
–
2.
Helper T cells
–
3.
Attack foreign cells or
virus-infected body cells
»
Commonly use
direct contact
Stimulate T cell and B cell
activation and function
Suppressor T cells
–
–
Inhibit T cell and B cell
activation and function
Work with helper T cells
to control immune
response sensitivity
Module 19.3: Lymphocytes
•
Lymphocyte classes
(continued)
–
B cells
•
When stimulated,
become plasma cells that
produce and secrete
antibodies
–
Antibodies then
circulate in body fluids
to attack targets
throughout the body
–
NK (natural killer) cells
•
•
Attack foreign cells,
virus-infected body
cells, and cancer cells
Provide continuous
monitoring of peripheral
tissues
The three classes of lymphocytes circulating in the bloodstream
Classes of Lymphocytes
T Cells
B Cells
NK Cells
Account for approximately 80 percent of circulating
lymphcytes; are of three major types
Account for 10–15 percent
of circulating lymphocytes
Account for 5–10
percent of
circulating
lymphocytes;
perform immune
surveillance,
attacking foreign
cells, body cells
infected with
viruses, and cancer
cells that appear in
normal tissues
Cytotoxic T Cells
Helper T Cells
Suppressor T Cells
Plasma Cells
Attack foreign cells
or body cells
infected by viruses,
commonly by direct
contact; are the
primary cells
involved in the
production of
cell-mediated
immunity (cellular
immunity)
Stimulate the
activation
and function
of both T cells
and B cells
Inhibit the activation
and function of both
T cells and B cells;
the interplay
between suppressor
T cells and helper T
cells helps establish
and control the
sensitivity of the
immune response
When stimulated can
differentiate into plasma
cells, which produce and
secrete antibodies; are
said to be responsible for
antibody-mediated
immunity (humoral
immunity) because
antibodies circulate widely
in body fluids
Figure 19.3
1
Module 19.3: Lymphocytes
• Lymphopoiesis (lymphocyte production)
– Occurs mainly in red bone marrow
•
Lymphocyte stem cells
–
–
Develop from hemocytoblasts
Produce all lymphocyte types from two groups
1. Group migrates to thymus
» Isolated by blood–thymus barrier
» Become T cells and reenter bloodstream
2. Group remains in bone to finish development
» Become B cells and NK cells
– Mature T cells and B cells can reproduce
Module 19.3 Review
a. Identify the three main
classes of lymphocytes.
b. Which cells are
responsible for antibodymediated immunity?
c . What tissues are involved
in lymphopoiesis?
Module 19.4: Lymphatic tissues and
organs
• Lymphatic tissues
– Connective tissues dominated by lymphocytes
•
May form aggregations of lymphocytes (lymphoid
nodules)
– Examples:
•
Aggregated lymphoid nodules (Peyer patches)
–
•
Deep to epithelium in small intestine
Mucosa-associated lymphoid tissue (MALT)
–
Protect epithelia of digestive, respiratory, urinary, and
reproductive tracts
A photomicrograph and a drawing of aggregated lymphoid nodules in the intestinal mucosa
An aggregated lymphoid nodule in the intestinal mucosa
Intestinal lumen
Mucous
membrane
of intestinal wall
Germinal center
Aggregated
lymphoid nodule
in intestinal mucosa
Underlying
connective tissue
Aggregated lymphoid
nodules
LM x 20
Figure 19.4
1
Module 19.4: Lymphatic tissues and
organs
• Tonsils
– Lymphoid nodules in pharynx wall
•
Inflammation of tonsils = tonsillitis
– Palatine (posterior, inferior margin of oral cavity)
•
Paired
– Pharyngeal (posterior, superior wall of pharynx)
•
•
Often called adenoid
Single
– Lingual (deep to epithelium at base of tongue)
•
Paired
The location and histology of tonsils
Germinal centers within nodules
Pharyngeal epithelium
The location of the tonsils
Pharyngeal tonsil
LM x 40
Pharyngeal tonsil
Hard palate
Palatine tonsil
Lingual tonsil
Figure 19.4
2
Module 19.4: Lymphatic tissues and
organs
• Lymph nodes
– Small lymphoid organs surrounded by fibrous
connective tissue capsule
– Diameter range 1–25 mm (about 1 in.)
– Large lymph nodes (lymph glands) located in neck,
groin, axillae
– Function as filters, removing 99% of pathogens from
lymph before fluid returns to bloodstream
Module 19.4: Lymphatic tissues and
organs
•
Pathway through lymph node
–
Afferent lymphatics (afferens, to bring to) bring lymph to node on
opposite side from hilum (indentation)
 Subcapsular space
–
•
–
 Outer cortex
•
–
B cells in germinal centers
 Deep cortex
•
–
T cells
 Medullary sinus
•
–
Macrophages and dendritic cells (immune response)
B cells and plasma cells
 Exit node through efferent (efferens, to bring out) lymphatics
Lymph node
Lymph vessel
Lymph nodes
The functional anatomy of lymph nodes
Path of Lymph Flow through a Lymph Node
Efferent lymphatics (efferens, to bring out)
leave the lymph node at the hilum. These
vessels collect lymph from the medullary sinus
and carry it toward the venous circulation.
Lymph node
artery and vein
Hilum
Lymph continues into the medullary sinus at
the core of the lymph node. This region
contains B cells and plasma cells.
Lymph then flows through lymph sinuses in the
deep cortex, which is dominated by T cells.
Lymph next flows into the outer cortex, which
contains B cells within germinal centers that
resemble those of lymphoid nodules.
The afferent vessels deliver lymph to the
subcapsular space, a meshwork of reticular
fibers, macrophages, and dendritic cells.
Dendritic cells are involved in the initiation of
the immune response.
Start
Afferent lymphatics (afferens, to bring to)
carry lymph to the lymph node from peripheral
tissues. The afferent lymphatics penetrate the
capsule of the lymph node on the side opposite
the hilum.
Germinal
center
Trabeculae
Figure 19.4
3
Module 19.4 Review
a. Define tonsil.
b. Name the lymphoid
tissue that protects
epithelia lining the
digestive, respiratory,
urinary, and
reproductive tracts.
Module 19.5: Thymus
• Function of the thymus and age-related
effects
– Produces several hormones (thymosins)
important in functional T cell development
• More important in children
– Size is largest (40 g) before puberty
– Diminishes in size and becomes fibrous (involution)
• After age 50, size can be <12 g and secretions decline
– May lead to increased susceptibility to disease
Module 19.5: Thymus
• Structure of the thymus
– Bilobed gland in mediastinum, posterior to sternum
• Left and right lobes with smaller partitions (septa)
dividing it into lobules
• Each lobule contains:
– Cortex (reticular epithelial cells and lymphocytes)
» Has blood–thymus barrier to isolate developing T cells
– Medulla (reticular epithelial cells and lymphocytes organized
into thymic corpuscles)
» Developed T cells enter bloodstream (no barrier)
The surface anatomy
of the thymus
Septa
Lobule
Left lobe
Right lobe
Figure 19.5
2
The histology of the thymus
Medulla
Septa
Cortex
Lobule
Lobule
LM x 50
Thymus gland
Lymphocytes
Thymic
corpuscle
Reticular epithelial
cells
Thymic corpuscle
LM x 532
Figure 19.5
3 – 4
Module 19.5 Review
a. Where is the thymus
located?
b. Which cells constitute
and maintain the
blood–thymus barrier?
c. Describe the gross
anatomy of the thymus.
Module 19.6: Spleen
• Similar to a lymph node:
filters blood for the body
to prevent pathogens
from reaching vital organs
• Extremely delicate tissue
– If damaged or ruptured it is
to difficult to fix surgically
and a slenectomy is usually
done
Spleen
A transverse section of the trunk showing the location of
the spleen within the abdominopelvic cavity
Diaphragm
Stomach
Rib
Gastrosplenic ligament
Liver
Gastric area
Pancreas
Aorta
Spleen
Kidneys
Diaphragmatic surface
of the spleen
Hilum
Renal area
Figure 19.6
1
Module 19.6: Spleen
•
Internal functional anatomy
–
Outer capsule of collagen and elastic fibers
•
Protects but overall spleen structure is delicate
–
–
Damage can necessitate removal (splenectomy)
Trabeculae
•
–
Fibrous partitions that allow room for blood vessels
Pulp (cellular components allowing identification and removal
of damaged or infected cells in bloodstream)
•
•
Red pulp (large quantities of RBCs)
White pulp (resemble lymphoid nodules with lymphocytes,
macrophages, and dendritic cells)
Trabeculae
Fibrous partitions within which blood
vessels travel
Capsule
Trabecula
Red pulp
Trabecular artery
White pulp of splenic nodule
Central artery in splenic nodule
The histological appearance of the spleen
LM x 50
Figure 19.6
4
Figure 19.6
5
Module 19.6 Review
a. What is the function of
the spleen?
b. Describe red pulp and
white pulp found in the
spleen.
.
Section 2: Nonspecific Defenses
• Two complementary mechanisms work to
fight infection, illness, and disease
1. Specific defenses (protect against particular
threats)
•
•
Depend on specific lymphocyte activities
Produce state of protection (immunity or specific
resistance)
Section 2: Nonspecific Defenses
•
Two complementary mechanisms work to fight infection,
illness, and disease (continued)
2.
Nonspecific defenses (present from birth and do not distinguish
one type of threat from another)
•
•
•
•
•
•
•
Physical barriers
Phagocytes
Immunological surveillance
Interferons
Complement
Inflammatory response
Fever
Animation: Immunity: Nonspecific Defenses
Module 19.7: Physical barriers and
phagocytes
• Physical barriers
– Integumentary system
• Secretions from sebaceous and sweat glands wash away
microorganisms and chemical agents
– May also contain bactericidal chemicals, destructive enzymes
(lysozymes), and antibodies
• Hair provides protection from mechanical abrasion and
prevents hazardous materials or insects from contacting
skin
• Multiple layers of epithelial cells with keratin that are
connected with desmosomes
Duct of eccrine
sweat gland
Hair
Secretion
Epithelium
Structures in the skin that constitute
a physical barrier
Keratinized
cells
Sebaceous
gland
Most epithelia are protected by
specialized accessory structures and
secretions. The epidermal surface
also receives the secretions of
sebaceous and sweat glands. These
secretions, which flush the surface to
wash away microorganisms and
chemical agents, may also contain
bactericidal chemicals, destructive
enzymes (lysozymes), and
antibodies.
Desmosomes
The hairs on most areas of your
body’s surface provide some
protection against mechanical
abrasion (especially on the scalp),
and they often prevent hazardous
materials or insects from
contacting your skin.
The epithelial covering of the skin
has multiple layers, a coating of
keratinized cells, and a network of
desmosomes that lock adjacent
cells together.
Figure 19.7
1
Module 19.7: Physical barriers and
phagocytes
• Physical barriers (continued)
– Other epithelial linings
• Found along digestive, respiratory, urinary, and
reproductive tracts
• Cells provide physical barrier
• Secretions (mucus, enzymes, stomach acid) often ensnare,
destroy, or wash away pathogenic material
The barrier provided by the epithelia lining the digestive, respiratory, urinary, and reproductive tracts
Mucus coating
Secretory cell
Mucus bathes most surfaces of your
digestive tract, and your stomach
contains a powerful acid that can
destroy many pathogens. Mucus
moves across the lining of the
respiratory tract, urine flushes the
urinary passageways, and glandular
secretions do the same for the
reproductive tract. Special enzymes,
antibodies, and an acidic pH add to
the effectiveness of these secretions.
Tight junctions
Basal lamina
Epithelial cells tied
together by tight
junctions and
supported by a
fibrous basal lamina
Figure 19.7
2
Module 19.7: Physical barriers and
phagocytes
• Phagocytes
– Engulf and destroy foreign compounds and pathogens
– “First line of cellular defense” against pathogenic invasion
– Types
1.
Neutrophils (in bloodstream and tissues)
–
2.
Eosinophils (less abundant)
–
3.
Phagocytize cellular debris or bacteria
Phagocytize foreign compounds and antibody-coated pathogens
Macrophages (derived from monocytes)
–
–
Fixed (permanent residents of certain organs)
Free (travel throughout body)
Types of Phagocytes
There are two major classes of macrophages derived from the
monocytes of the circulating blood. This collection of phagocytic
cells is called the monocyte–macrophage system, or the
reticuloendothelial system.
12 μm
8–10 μm
Neutrophils are
abundant, mobile,
and quick to
phagocytize cellular
debris or invading
bacteria. They
circulate in the
bloodstream and
roam through
peripheral tissues,
especially at sites
of injury or
infection.
Eosinophils, which
are less abundant
than neutrophils,
phagocytize foreign
componds or
pathogens that have
been coated with
antibodies.
Fixed macrophages are permanent
residents of specific tissues and organs
and are scattered among connective
tissues. They normally do not move within
these tissues.
Free macrophages travel
throughout the body, arriving at the
site of an injury by migrating through
adjacent tissues or by recruitment
from the circulating blood.
Figure 19.7
3
Figure 19.7
4
Module 19.7 Review
a. Define chemotaxis.
b. How does the
integumentary system
protect the body?
c. Identify the types of
phagocytes in the body,
and differentiate
between fixed
macrophages and free
macrophages.
Module 19.8: Immunological
surveillance
• Immunological surveillance
– Constant monitoring of normal tissues by NK cells
•
•
Normal cells are generally ignored by immune system
Cancer cells often contain tumor-specific antigens
–
•
NK cells recognize as abnormal and destroy
NK cells recognize bacteria, foreign cells, virus-infected
cells, and cancer cells
Module 19.8: Immunological
surveillance
•
Steps of NK recognition and destruction
1.
Presence of unusual plasma membrane activates
NK cell
•
2.
NK cell adheres to target cell
Golgi apparatus moves within NK cell near target cell
•
3.
4.
Produces many secretory vesicles containing perforins
Perforins release from NK cell and arrive at target cell
Perforins create pores in target cell membrane
•
Target cell can no longer maintain its internal environment and
disintegrates
The steps by which NK cells recognize and kill target cells
Step 1: If a cell has
unusual components in its
plasma membrane, an NK
cell recognizes that other
cell as abnormal. Such
recognition activates the
NK cell, which then
adheres to its target cell.
Step 2: The Golgi apparatus
moves around the nucleus until
the maturing face points directly
toward the abnormal cell. A flood
of secretory vesicles is then
produced at the Golgi apparatus.
These vesicles, which contain
proteins called perforins, travel
through the cytoplasm toward the
cell surface.
Step 3: The perforins
are released at the cell
surface by exocytosis
and diffuse across the
narrow gap separating
the NK cell from its
target.
Step 4: As a result of the
pores made of perforin
molecules, the target cell
can no longer maintain
its internal environment,
and it quickly
disintegrates.
Golgi apparatus
NK cell
Abnormal
cell
Perforin
molecules
NK cell
Pores produced by the
interaction of perforin
molecules
Abnormal
cell
Figure 19.8
1
Module 19.8: Immunological
surveillance
•
NK cells also destroy
abnormal cells
–
–
Abnormal daughter cells
occur during cell division
Some abnormal cells
become cancer cells
The process whereby NK cells detect
and destroy abnormal cells
resulting from faulty
cell division
Abnormal cell
NK cell identifies and
destroys abnormal cell
Stem cell
Daughter cells
Daughter cells
Figure 19.8
2
Module 19.8: Immunological
surveillance
• Immunological escape
– Immunological surveillance by NK cells is not
perfect
•
Primary tumors may be surrounded by a capsule and
escape detection
–
•
Released malignant cells may be detected and destroyed
Daughter tumor cells sometimes do not display tumorspecific antigens or secrete chemicals that kill NK cells
–
Cancer cells can spread and create secondary tumors
The process of immunological escape
NK cell
The cells within a primary
tumor may grow rapidly,
and if the tumor has a
surrounding capsule, the
cells within may not
provoke a massive
response by NK cells.
As malignant tumor
cells begin migrating
into surrounding
tissues, they can be
detected and
destroyed by NK cells.
Sometimes a daughter cell will be
produced that either does not
display tumor-specific antigens, or
that secretes chemicals that
destroy NK cells. Such a cell will
survive and be free to grow and
divide.
Once immunological
escape has occurred,
cancer cells can
multiply and spread
without interference by
NK cells. They can then
move throughout the
body, establishing
potentially lethal
secondary tumors.
Figure 19.8
3
Module 19.8 Review
a. Define immunological
surveillance.
b. How do NK cells detect
cancer cells?
c. If NK cells are engaged in
immunological
surveillance, how do
cancer cells spread?
Module 19.9: Interferons and the
complement system
• Interferons
– Small proteins released by activated lymphocytes,
macrophages, and virus-infected tissues
– Trigger antiviral proteins in cytoplasm of nearby
cells
•
Do not prevent entry of viruses but interfere with viral
replication
– Also stimulate activities of macrophages and NK
cells
Module 19.9: Interferons and the
complement system
• Interferons (continued)
– Three types
1. Alpha (α) interferons (produced by virus-infected cells)
–
Attract and stimulate NK cells and give viral resistance
2. Beta (β) interferons (secreted by fibroblasts)
–
Slow inflammation in damaged area
3. Gamma (γ) interferons (secreted by T cells and NK cells)
–
Stimulate macrophage activity
Three of the types of interferons
Alpha (α)-interferons
are produced by cells
infected with viruses.
They attract and
stimulate NK cells and
enhance resistance to
viral infection.
Beta (β)-interferons,
secreted by fibroblasts,
slow inflammation in a
damaged area.
Gamma
()-interferons,
secreted by T cells and
NK cells, stimulate
macrophage activity.
Figure 19.9
1
Module 19.9: Interferons and the
complement system
•
Complement system (complements antibody action)
–
–
11 plasma proteins that interact to attach to foreign cells
Two pathways of activation
1.
Classical pathway (most rapid and effective)
–
–
2.
Complement proteins attach to antibody already bound to pathogen
Attached protein activates and initiates cascade to activate and
attach other complement proteins
Alternative pathway
–
Several complement proteins (notably properdin) activate in plasma
after contacting foreign materials
Module 19.9: Interferons and the
complement system
•
Complement system effects
–
Pore formation (formed by many complement proteins)
•
–
Destroys integrity of target cell
Enhanced phagocytosis
•
Attracts phagocytes and makes target cells easier to engulf
–
–
= Opsonization
Histamine release
•
•
By mast cells and basophils
Increases inflammation and blood flow to region
Animation: Immunity: Complement
Module 19.9 Review
a. Define interferons.
b. Briefly explain the role of complement
proteins.
c. What is the effect of histamine released by
complement system activation?
Module 19.10: Inflammation and
fever
• Inflammatory response
– Localized tissue response that produces:
•
•
•
•
Local swelling
Redness
Heat
Pain
– Complex process of inflammation can be triggered by:
•
•
Cells that are damaged from any source release
prostaglandins, proteins, and potassium ions
Foreign proteins or pathogens
Module 19.10: Inflammation and fever
•
The events in inflammation
–
–
Tissue damage causes chemical change in interstitial fluid
Mast cell activation
•
Release of histamine and heparin
–
–
Causes:
» Increased blood flow to area
» Clot formation
» Phagocyte attraction (removes debris and activates specific
defenses)
Tissue repair
•
Pathogen removal, clot erosion, scar tissue formation
Module 19.10: Inflammation and fever
• Fever
– Maintenance of body temperature >37.2°C (99°F)
– Pyrogens (pyro-, fever or heat, + -gen, substance)
•
Reset temperature thermostat in hypothalamus
–
•
Raises body temperature
Functions
–
–
May inhibit some viruses and bacteria
Increases metabolic rate which may accelerate tissue defenses
and repair process
A summary of the body’s nonspecific defenses
Physical Barriers
Prevent approach of
and deny access to
pathogens
Secretions
Epithelium
Duct of eccrine
sweat gland
Hair
Phagocytes
Remove debris
and pathogens
Neutrophil
Eosinophil
Monocyte
Free
macrophage
Fixed
macrophage
Immunological Surveillance
Destroys
abnormal cells
Lysed
abnormal
cell
Natural killer cell
Interferons
Increase resistance of
cells to viral infection;
slow the spread of
disease
Interferons released by activated
lymphocytes, macrophages, or
virus-infected cells
Figure 19.10 3
A summary of the body’s nonspecific defenses
Complement System
Attacks and breaks down the
surfaces of cells, bacteria, and
viruses; attracts phagocytes;
stimulates inflammation
Lysed
pathogen
Complement
Inflammatory Response
Multiple effects
Mast cell
• Blood flow increased
• Phagocytes activated
• Damaged area isolated by clotting reaction
• Capillary permeability increased
• Complement activated
• Regional temperature increased
• Specific defenses activated
Fever
Mobilizes defenses;
accelerates repairs;
inhibits pathogens
Body temperature rises above 37.2°C in
response to pyrogens
Figure 19.10 3
Module 19.10 Review
a. List the body’s nonspecific defenses.
b. A rise in the level of interferons in the body
suggests what kind of infection?
c. What effects do pyrogens have in the body?
Section 3: Specific Defenses
• Specific defenses
– Coordinated activities of T cells and B cells
•
Produce immunity
–
•
T cells (cell-mediated immunity)
–
•
Specific resistance against potentially dangerous antigens
Defend against abnormal cells and pathogens inside cells
B cells (antibody-mediated immunity)
–
Defend against antigens and pathogens in body fluids
The various forms of immunity
Specific Defenses (Immunity)
Respond to threats on an
individualized basis
Aquired Immunity
Innate Immunity
Is not present at birth; is acquired
against a specific antigen only upon
exposure to that antigen or receipt of
antibodies from some
other source
Genetically
determined—no
prior exposure
or antibody
production
involved
Passive Immunity
Active Immunity (Immune Response)
Produced by
transfer of
antibodies from
another source
Develops in
response to antigen
exposure
Naturally
acquired
passive
immunity
Artificially
acquired
passive
immunity
Naturally
acquired
active
immunity
Conferred by
transfer of
maternal
antibodies across
placenta or in
breast milk
Conferred by
administration of
antibodies to
combat infection
Develops after
exposure to
antigens in
environment
Artificially acquired
active immunity
Develops after
administration of an antigen
(usually through
vaccination). These
activities stimulate an
immune response and
promote immunity to that
particular antigen.
Figure 19 Section 3 1
Section 3: Specific Defenses
• Properties of immunity
1. Specificity
•
T cells and B cells bind only one antigen
2. Versatility
•
Millions of lymphocytes, each sensitive to a different
antigen
3. Immunologic memory
•
Memory cells “remember” antigens for future attacks
4. Tolerance
•
Ignoring normal “self” tissues
Module 19.11: Triggering an immune
response
• Phagocytes activated by antigen exposure
stimulate specific immune responses
• To trigger a response, antigens or antigenic
fragments must appear in plasma
membranes from:
– Infecting cells or being “processed” by
phagocytes
• = Antigen presentation
An overview of the immune response
Antigens or Antigenic
Fragments in Body Fluids
Most antigens must either
infect cells or be
“processed” by
phagocytes before specific
defenses are activated. The
trigger is the appearance
of antigens of antigenic
fragments in plasma
membranes;
this is called antigen
presentation.
Cell-Mediated
Immunity
Direct Physical and
Chemical Attack
Phagocytes
activated
Activated T cells find
the pathogens and
attack them through
phagocytosis or the
release of chemical
toxins.
Specific Defenses
Antigen
presentation
triggers specific
defenses, or an
immune response.
T cells
activated
Destruction
of antigens
Communication
and feedback
Antibody-Mediated
Immunity
Attack by Circulating
Antibodies
Activated B
cells give
rise to cells
that produce
antibodies.
Figure 19.11 1
Module 19.11: Triggering an immune
response
• Major histocompatibility complex (MHC)
proteins
– Genetically determined membrane glycoproteins
present on all cells
•
Synthesis controlled by portion of chromosome 6
–
= Major histocompatibility complex
– Foreign antigens are attached to newly synthesized
MHC proteins and appear on cell surface
– T cells bind antigen-MHC complex and become
activated
Module 19.11: Triggering an immune
response
• MHC proteins
– Two classes
1. Class I MHC proteins
–
–
Present on all cells
Create complex when cell is infected with bacteria or viruses
2. Class II MHC proteins
–
–
Only in membranes of antigen-presenting cells (APC)
» Examples: monocyte–macrophages, dendritic cells
Create complex with phagocytized pathogens
The events of antigen presentation in an infected body cell
Plasma membrane
Antigen presentation
by Class I MHC
proteins is triggered
by viral or bacterial
infection of a body
cell.
Viral or bacterial
pathogen
Transport
vesicle
The infection results
in the appearance of
abnormal peptides in
the cytoplasm.
The abnormal
peptides are
incorporated into
Class I MHC proteins
as they are
synthesized at the
endoplasmic
reticulum.
The abnormal
peptides are
displayed by Class
I MHC proteins on
the plasma
membrane.
Endoplasmic
reticulum
After export to the
Golgi apparatus,
the MHC proteins
reach the plasma
membrane within
transport vesicles.
Figure 19.11 2
The events of antigen presentation in a phagocytic cell
Plasma
membrane
Phagocytic APCs
engulf the
extracellular
pathogens.
Antigenic fragments
are displayed by Class
II MHC proteins on the
plasma membrane.
Antigenic fragments
are bound to Class II
MHC proteins.
Lysosomal action
produces antigenic
fragments.
The endoplasmic
reticulum produces
Class II MHC proteins.
Lysosome
Nucleus
Endoplasmic
reticulum
Phagocytic cell
Figure 19.11 3
Module 19.11 Review
a. Describe antigen presentation.
b. What is the major histocompatibility
complex (MHC)?
c. Where are Class I MHC proteins and Class II
MHC proteins found?
Module 19.12: T cell activation by
infected cells
• Inactive T cells must bind the specific MHCantigen complex that the T cell is programmed
to detect
– = Antigen recognition
– Two classes of T cell CD (cluster of differentiation)
markers can recognize antigens
1. CD8 markers (on CD8 T cells)
–
Respond to Class I MHC proteins
2. CD4 markers (on CD4 T cells)
–
Respond to Class II MHC proteins
The structures involved in the process of
antigen recognition
Inactive T cell
Receptor
Antigen
recognition
protein
Antigen
MHC protein
Infected body cell (including APCs)
Figure 19.12 1
CD (cluster of differentiation) markers, the membrane
proteins involved in antigen recognition
CD Markers
There are at least 70 different
CD markers, but only two
associated with T cells are
important to our discussion.
CD8 Markers
CD4 Markers
CD8 markers are
found on CD8 T cells.
CD8 T cells respond to
antigens presented by
Class I MHC proteins.
CD4 markers are
found on CD4 T cells.
CD4 T cells, discussed
further in the next
module, respond to
antigens presented by
Class II MHC proteins.
Figure 19.12 2
Module 19.12: T cell activation by
infected cells
• Steps of CD8 T cell activation
1. Antigen recognition
2. Costimulation
•
Physical or chemical stimulation of T cell in addition to
the Class I MHC molecule
3. T cell activation and cell division
•
Three CD8 T cells produced
1.
2.
3.
Cytotoxic T cells (TC cells)
Memory TC cells
Suppressor T cells (TS cells)
Events in the stimulation and formation of cytotoxic, memory TC, and suppressor T cells
Cytotoxic T Cells Seek Out Antigen-Bearing Cells
Activation and
Cell Division
Antigen Recognition
Antigen recognition occurs
when a CD8 T cell encounters
an appropriate antigen on the
surface of another cell, bound
to a Class I MHC protein.
Infected
cell
Viral or
bacterial
antigen
Antigen
recognition
results in T cell
activation and cell
division,
producing three
different types of
CD8 T cells.
Inactive
CD8
T cell
Cytotoxic T cells, also called TC cells, seek out and destroy
abnormal and infected cells. Cytotoxic T cells are highly mobile cells
that roam throughout injured tissues. When a T C cell encounters its
target antigens bound to Class I MHC proteins, it attacks the target
cell.
Destruction of Target Cells
The TC cell destroys the antigenbearing cell. It may use several
different mechanisms to kill the
target cell.
Memory TC Cells Are Produced
Memory TC cells are produced by
the same cell divisions that produce
cytotoxic T cells. Thousands of these
cells are produced, but they do not
differentiate further the first time the
antigen triggers an immune
response.
Costimulation
Suppressor T Cells Provide a Delayed Suppression
Costimulation
activates
CD8 T cell
CD8
Class I
MHC
T cell
receptor
Antigen
Infected cell
Memory TC cells
(inactive)
Suppressor T cells (TS cells)
suppress the responses of other T
cells and B cells by secreting
suppression factors that limit the
degree of immune system activation.
Suppression does not occur
immediately, because suppressor T
cell activation takes much longer
than the activation of other types of T
cells, and so suppressor T cells act
only after the initial immune
response.
Destruction of target cell
membrane through the
release of perforins
Activation of genes within the
target cell nucleus that results
in the self-destruction of the
cell through a process called
apoptosis (ap-op-TŌ-sis)
Disruption of cell metabolism
through the release of
lymphotoxin (lim-fō-TOK-sin)
Suppressor
T cells
CD8 T cell
Before activation can occur, a T cell must
be chemically or physically stimulated by
the abnormal target cell. This vital
secondary binding process, called
costimulation, confirms the activation
signal. Costimulation is like the safety on a
gun: It helps prevent T cells from
mistakenly attacking normal (self) tissues.
Figure 19.12 3 – 4
Module 19.12: T cell activation by infected
cells
• CD8 T cell types
1. Cytotoxic TC cells
•
Seek out and destroy abnormal and infected cells in
injured tissues
–
–
Target cells must have specific Class I MHC proteins
Destructive mechanisms
» Release of perforins
» Activate target cell self-destruction genes for cell death
(apoptosis)
» Disruption of cell metabolism with lymphotoxin
Module 19.12: T cell activation by
infected cells
•
CD8 T cell types (continued)
2.
Memory TC cells
•
•
3.
Produced but do not differentiate further during first antigen
exposure
Upon 2nd exposure to same antigen, memory TC cells become
cytotoxic T cells
Suppressor T cells
•
•
Secrete suppression factors to limit responses of other T cells and B
cells
Also act only after first antigen exposure (initial immune response)
Module 19.12 Review
a. Identify the three major
types of T cells
activated by Class I MHC
proteins.
b. Describe CD markers.
c. How can the presence of
an abnormal antigen in
the cytoplasm of a cell
initiate an immune
response?
Module 19.13: CD4 T cell and B cell
activation
•
B cell activation
–
–
Must bind specific antigen
Antigens are brought into cell through endocytosis and then placed
on surface of cell bound to Class II MHC proteins
•
–
= Sensitization
Full activation occurs when activated helper T cell binds to
sensitized B cell antigen-Class II MHC complex
Activated B cells produce:
–
•
•
Memory B cells (inactive until 2nd exposure to antigen)
Plasma cells (activated B cells that produce antibodies)
Module 19.13: CD4 T cell and B cell
activation
Animation: B Cell Sensitization
The process whereby stimulation of CD4 T cells results in the production of antibodies
Antigen Recognition by CD4 T Cell
Foreign antigen
Antigen
Class II MHC
Antigens
Antigen-presenting
cell (APC)
Class II MHC
B Cell Activation
B Cell Sensitization
Class II MHC
APC
Antigen
Inactive
B cell
Inactive
CD4 (TH)
cell
Sensitized B cell
Costimulation
by cytokines
T cell receptor
Antibodies
Costimulation
CD4 protein
Division, Differentiation, and Antibody Production
Antigens bound
to antibody
molecules
Sensitized
B cell
Memory B cells
(inactive)
Memory B cells remain in
reserve to deal with subsequent
injuries of infections that
involve the same antigens. On
subsequent exposure, the
memory B cells respond by
differentiating into plasma cells
that secrete antibodies in
massive quantities.
Helper T cell
Sensitized
B cell
Activated
B cell
T cell receptor
Cell
division
TH cell
The Golgi apparatus is
packaging membrane
receptors (red) that will be
incorporated into the surface
of the cell. These receptors
are essential to the
costimulation of B cells.
CD4 T Cell Activation and Cell Division
Cytokines
Active B cells
Active
helper T cell
Stimulation
by cytokines
Active
helper T cell
Memory TH cells
(inactive)
Plasma cells
Cytokines
Active helper T cells
Active helper T cells secrete
cytokines that stimulate
both cell-mediated and
antibody-mediated immunity.
Under stimulation
by cytokines from
helper T cells,
clones of active B
cells differentiate
into plasma
cells, each
capable of
secreting up to
100 million
antibody
molecules each
hour.
Antibody
molecules
An activated helper T cell
Fluorescent LM x 400
Figure 19.13
Module 19.13 Review
a. Define sensitization.
b. Explain the function of
cytokines secreted by
helper T cells.
c. If you observed a higherthan-normal number of
plasma cells in a sample
of lymph, would you
expect antibody levels in
the blood to be higher or
lower than normal?
Module 19.14: Antibodies
• Antibody molecules
– Consist of two parallel polypeptide chains
•
•
One pair of heavy chains
One pair of light chains
– Each pair contains:
•
Constant segments
–
•
On heavy chains, form the base of antibody molecule
Variable segments
–
–
Free tips are antigen binding sites
Differences in amino acid sequences produce variability needed
for different antibodies
The structure of an antibody molecule
Antigen
binding
site
Variable
segment
Antigen binding sites
Heavy chain
Disulfide
bond
Light chain
Constant
segments
of light
and heavy
chains
Binding sites that can activate the complement system
are covered when the antibody is secreted but become
exposed when the antibody binds to an antigen.
Binding sites may also be present that attach the
secreted antibody to the surfaces of macrophages,
basophils, or mast cells.
Figure 19.14 1
Module 19.14: Antibodies
•
Antigen-antibody complex
–
When a specific antibody binds to corresponding antigenic
determinant sites (binding sites) on antigen
• Complete antigens
–
–
•
Have at least two antigenic determinant sites, one for each binding site
on antibody
Large antigens (like bacteria) may have millions of antigenic determinant
sites
Partial antigens (haptens)
–
–
Do not have enough binding sites to bind antibody
Antibody may bind to hapten and carrier molecule
»
Response will then be against body cell carrier molecule as well
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
A bacterium with numerous antigenic
determinant sites, to which antibodies bind
Antigen
Antigenic
determinant sites
Antibodies
Figure 19.14 3
Module 19.14: Antibodies
•
Five different classes of antibodies (immunoglobulins or Igs)
–
1.
Differences in heavy-chain constant segments
IgG (80% of all antibodies)
•
2.
Against many viruses, bacteria, and bacterial toxins
IgE
•
3.
Attaches to basophil and mast cell surfaces
IgD
•
•
On B cell surface where it binds antigens in extracellular fluid
Plays role in B cell sensitization
Module 19.14: Antibodies
• Five different classes of antibodies (continued)
4. IgM
•
First class of antibody secreted after antigen
encountered
–
•
Production declines as IgG production increases
Anti-A and anti-B antibodies are examples
5. IgA
•
•
Found primarily in glandular secretions such as mucus,
tears, saliva, and semen
Attack before pathogens gain internal access
The five classes of antibodies, or immunoglobulins (Igs)
Classes of Antibodies
IgG antibodies
account for 80 percent
of all antibodies. IgG
antibodies are
responsible for
resistance against
many viruses,
bacteria, and baterial
toxins.
IgE attaches as
an individual
molecule to the
exposed
surfaces of
basophils and
mast cells.
IgD is an individual
molecule on the
surfaces of B cells,
where it can bind
antigens in the
extracellular fluid. This
binding can play a role
in the sensitization of
the B cell involved.
IgM is the first class of
antibody secreted after an
antigen is encountered. IgM
concentration declines as IgG
production accelerates. The
anti-A and anti-B antibodies
responsible for the
agglutination of incompatible
blood types are IgM
antibodies.
IgA is found primarily
in glandular secretions
such as mucus, tears,
saliva, and semen.
These antibodies attack
pathogens before they
gain access to internal
tissues.
Figure 19.14 4
Module 19.14: Antibodies
• Primary response
– Antibody-mediated response to initial antigen
exposure
– Is delayed due to time to activate specific B cells
•
Antibody titer (level of antibody activity) peaks
1–2 weeks after initial exposure
• Secondary response
– From memory B cells for specific antigen
– Antibody titers increase more rapidly and reach
higher concentrations
The time course and amount of antibody production for an initial exposure to an antigen and for a
subsequent exposure to the same antigen
Antibody concentration
in plasma
Primary response
Secondary response
IgG
IgG
IgM
Time (weeks)
A primary antibody response, which occurs after
an initial exposure to an antigen
IgM
Time (weeks)
A secondary antibody response, which occurs after
the eliciting antigen has been encountered before
Figure 19.14 5 – 6
Module 19.14 Review
b. Describe the structure of an antibody.
c. Which would be more affected by a lack of
memory B cells and memory T cells: the
primary response or the secondary
response?
Module 19.15: Antibody defenses
• Antibody defenses
– Neutralization
• Antibodies occupy binding sites on viruses and bacterial
toxins preventing them from affecting body cells
– Prevention of pathogen adhesion
• IgA antibodies in glandular secretions cover bacteria or
viruses preventing adhesion and infection of body cells
– Activation of complement
• After antigen binding, complement also can bind to the
antibody, accelerating the complement cascade
Module 19.15: Antibody
defenses
• Antibody defenses (continued)
– Stimulation of inflammation
•
Basophil and mast cell stimulation to release chemicals
– Opsonization
•
Coating of pathogen with antibodies allows phagocytes
to bind easier
– Attraction of phagocytes
•
Attached antibodies attract eosinophils, neutrophils,
and macrophages
Module 19.15: Antibody
defenses
• Antibody defenses (continued)
– Precipitation and agglutination
• The linking of multiple pathogens by antibodies creating
an immune complex
– When target antigen is on cell surface (like RBC) or virus
» = Agglutination
Module 19.15 Review
a. Define opsonization.
b. List the ways that antigen-antibody
complexes can destroy target antigens.
c. Which cells are involved in the
inflammatory response?
CLINICAL MODULE 19.16: Allergies
•
Allergies
–
Inappropriate or excessive immune responses to antigens
(allergens)
Sensitization and activation of B cells to allergens leads to
production of large quantities of IgE
Reactions may be:
–
–
•
Localized (inflammation, pain, itching at contact area)
–
•
Example: hypersensitivity reaction of allergic rhinitis (hay fever and
other environmental allergies)
Systemic (allergen in bloodstream, symptoms widespread)
–
Example: anaphylaxis (circulating allergen causing widespread
vasodilation through mast cell activation)
The events that result in an allergy
First Exposure
Allergen fragment
Allergens
TH cell activation
Macrophage
B cell sensitization
and activation
Plasma cell
IgE antibodies
Subsequent
Exposure
IgE
Allergen
Massive
stimulation of
mast cells
and basophils
Granules
Sensitization of
mast cells and
basophils
Release of histamines, leukotrienes,
and other chemicals that
cause pain and inflammation
Localized Allergic Reactions
Systemic Allergic Reactions
If the allergen is at the body
surface: localized inflammation,
pain, and itching
Example: allergic rhinitis
If the allergen is in the
bloodstream: itching, swelling,
and difficulty breathing (due to
airway constriction)
Example: anaphylaxis
Figure 19.16
CLINICAL MODULE 19.16 Review
a. Define allergy and allergen.
b. What is anaphylaxis?
c. Which chemicals do mast cells and
basophils release when stimulated in an
allergic reaction?
Module 19.17: Integrated defense
responses
• Exposure to antigens triggers both specific
and nonspecific defenses
– Neither branch works alone
– Many times, activities from each branch will
enhance the other
• Responses will vary based on antigen type
The relationships among the elements of the nonspecific defenses and the specific defenses (immune response)
Antigens
Trigger
Nonspecific Defenses
Complement
system
NK cells
Macrophages
Specific Defenses (Immune Response)
Antigen
presentation
by APCs
Activation by Class I MHC Proteins
Activation by Class II MHC Proteins
Antigen and
Class I MHC
Protein
Antigen and
Class II MHC
Protein
Indicates that the
cell is infected or
otherwise abnormal
CD8 T cells
Cytotoxic
T Cells
Memory
Tc Cells
Suppressor
T Cells
Attack and
destroy infected
and abnormal
cells displaying
antigen
Await
reappearance
of the antigen
Control of
moderate
immune response
by T cells and B
cells
Helper T Cells
Memory TH Cells
Stimulate immune
response by T
cells and B cells
Await
reappearance of
the antigen
Production
of memory B
cells
Production of
plasma cells
Direct physical
and chemical
attack
Attack by
circulating
proteins
CD4 T cells
Activation
of B cells
Direct physical
and chemical
attack
Indicates the
presence of
pathogens,
toxins, or foreign
proteins
Destruction
of Antigens
Secretion of
antibodies
Figure 19.17 1
An overview of the course of events
involved in overcoming a bacterial infection
BACTERIA
Phagocytosis by
macrophages and APCs
Antigen
presentation
Activation of
cytotoxic T cells
Activation of
helper T cells
Activation
of B cells
Destruction of
bacteria by
cell lysis
Antibody
production by
plasma cells
Opsonization
and phagocyte
attraction
Formation of
antigen-antibody
complexes
Figure 19.17 2
An overview of the course of events involved in overcoming a
viral infection
VIRUSES
Release of
interferons
Increased
resistance to
viral infection
and spread
Infection of
tissue cells
Infection of or uptake
by APCs
Appearance of antigen
in plasma membrane
Antigen
presentation
Stimulation
of NK cells
Activation of
cytotoxic T cells
Destruction of
virus-infected cells
Destruction of
viruses or
prevention of
virus entry into cells
Activation of
helper T cells
Activation
of B cells
Antibody
production by
plasma cells
Figure 19.17 3
Module 19.17 Review
a. Identify the type of T cell whose plasma
membrane contains CD8 markers and the
type with CD4 markers.
b. Which cells can be activated by direct
contact with virus-infected cells?
c. Which cells produce antibodies?
CLINICAL MODULE 19.18: Immune
disorders
• Excessive or misdirected immune responses
– Autoimmune disorders
•
Activated B cells make antibodies against “self”
antigens or body cells and tissues
–
•
= Autoantibodies
Likely arise from body cell antigens being too similar
to specific foreign antigen
CLINICAL MODULE 19.18: Immune
disorders
• Excessive or misdirected immune responses
(continued)
– Autoimmune disorders (continued)
•
Examples:
–
–
–
–
Thyroiditis (inflammation resulting from autoantibodies
attacking thyroglobin)
Rheumatoid arthritis (autoantibodies attack connective tissues
around joints)
Insulin-dependent diabetes mellitus (autoantibodies attack
pancreatic islet cells)
Multiple sclerosis (autoantibodies attack myelin)
CLINICAL MODULE 19.18: Immune
disorders
• Excessive or misdirected immune responses
(continued)
– Graft rejection
•
•
Recipient cytotoxic T cells become activated and attack
MHC proteins of donated material
Reduction in immune response sensitivity
(immunosuppression) by drugs can increase transplant
success
–
Example: cyclosporin A (CsA) inhibits helper T cells
– Allergies
CLINICAL MODULE 19.18: Immune
disorders
• Inadequate immune responses
– Immunodeficiency diseases
•
Result from:
1.
2.
3.
Problems with lymphoid organ and tissue development
An infection with a virus that depresses immune function
» Example: Acquired immune deficiency syndrome caused
by human immunodeficiency virus (HIV) that infects CD4 T
cells
Treatment with, or exposure to, immunosuppressive agents like
radiation or drugs
CLINICAL MODULE 19.18: Immune
disorders
• Inadequate immune responses (continued)
– Age-related reductions in immune activity
•
T cells become less responsive
–
•
B cell response also less due to number of helper T
cells reduced
–
•
Fewer cytotoxic T cells respond
» Possibly related to thymus involution
Vaccinations highly recommended
NK cells reduced and immune surveillance
compromised
–
Increased incidence of cancer
CLINICAL MODULE 19.18 Review
a. Define autoimmune disorders.
b. Describe immunosuppression.
c. Provide a plausible explanation for the
increased incidence of cancer in the elderly.