CH 12 Lymphatic-System

Chapter 12
The Lymphatic
System and Body
Defenses
Lecture Presentation by
Patty Bostwick-Taylor
Florence-Darlington Technical College
© 2018 Pearson Education, Inc.

Part I: The Lymphatic System
 Consists of two semi-independent parts:

1. Lymphatic vessels
2. Lymphoid tissues and organs
 Lymphatic system functions
 Transports escaped fluids from the cardiovascular
system back to the blood
 Plays essential roles in body defense and resistance
to disease

Lymphatic Vessels
 Lymph consists of excess tissue fluid and plasma

proteins carried by lymphatic vessels
 If fluids are not picked up, edema occurs as fluid
accumulates in tissues
 Lymphatic vessels (lymphatics) pick up excess
fluid (lymph) and return it to the blood

Figure 12.1 Relationship of lymphatic vessels to blood vessels.
Venous Arterial
system system
Heart
Lymph duct
Lymph trunk
Lymph node
Lymphatic
system
Lymphatic
collecting
vessels,
with valves
Lymph
capillary
Tissue fluid
(becomes
lymph)
Blood Loose connective

capillaries tissue around
capillaries
Lymphatic Vessels
 Lymphatic vessels (lymphatics)

 Form a one-way system
 Lymph flows only toward the heart

Lymphatic Vessels
 Lymph capillaries
 Weave between tissue cells and blood capillaries
 Walls overlap to form flaplike minivalves
 Fluid leaks into lymph capillaries
 Capillaries are anchored to connective tissue by
filaments
 Higher pressure on the inside closes minivalves
 Fluid is forced along the vessel

Figure 12.2a Special structural features of lymphatic capillaries.
Tissue fluid
Tissue cell
Lymphatic
capillary
Blood
capillaries
(a) Arteriole Venule

Figure 12.2b Special structural features of lymphatic capillaries.
Fibroblast in loose
connective tissue
Flaplike
minivalve
Filaments
anchored to
Endothelial connective
cell tissue
(b)
Lymphatic Vessels
 Lymphatic collecting vessels

 Collect lymph from lymph capillaries
 Carry lymph to and away from lymph nodes
 Return fluid to circulatory veins near the heart
 Right lymphatic duct drains the lymph from the right arm
and the right side of the head and thorax
 Thoracic duct drains lymph from rest of body

Figure 12.3 Distribution of lymphatic vessels and lymph nodes.
Entrance of right
Regional lymphatic duct into right
lymph nodes: subclavian vein
Cervical Internal jugular vein

nodes
Thoracic duct
entry into left
subclavian vein
Axillary
nodes
Thoracic duct
Aorta
Spleen
Cisterna chyli (receives
lymph drainage from
Inguinal digestive organs)
nodes
Lymphatics
KEY:
Drained by the right lymphatic duct
Drained by the thoracic duct
Lymphatic Vessels
 Lymphatic vessels are similar to veins of the

cardiovascular system
 Thin-walled
 Larger vessels have valves
 Low-pressure, pumpless system
 Lymph transport is aided by:
 Milking action of skeletal muscles
 Pressure changes in thorax during breathing
 Smooth muscle in walls of lymphatics

Lymph Nodes
 Lymph nodes filter lymph before it is returned to

the blood
 Harmful materials that are filtered
 Bacteria
 Viruses
 Cancer cells
 Cell debris

Lymph Nodes
 Defense cells within lymph nodes

 Macrophages—engulf and destroy bacteria, viruses,
and other foreign substances in lymph
 Lymphocytes—respond to foreign substances in lymph

Lymph Nodes
 Most lymph nodes are kidney-shaped, less than

1 inch long, and buried in connective tissue
 Surrounded by a capsule
 Divided into compartments by trabeculae
 Cortex (outer part)
 Contains follicles—collections of lymphocytes
 Germinal centers enlarge when antibodies are
released by plasma cells
 Medulla (inner part)
 Contains phagocytic macrophages

Figure 12.4 Structure of a lymph node.
Germinal
center in
Afferent follicle Capsule
lymphatic
vessels Subcapsular
sinus
Trabecula
Afferent
Efferent
lymphatic
lymphatic
vessels
vessels
Hilum
Cortex
Medullary sinus
Follicle
Medullary cord

Lymph Nodes
 Flow of lymph through nodes

 Lymph enters the convex side through afferent
lymphatic vessels
 Lymph flows through a number of sinuses inside the
node
 Lymph exits through efferent lymphatic vessels
 Because there are fewer efferent than afferent vessels,
flow is slowed

Other Lymphoid Organs
 Several other lymphoid organs contribute to

lymphatic function (in addition to the lymph
nodes)
 Spleen
 Thymus
 Tonsils
 Peyer’s patches
 Appendix

Figure 12.5 Lymphoid organs.
Tonsils (in
pharyngeal region)
Thymus (in thorax;

most active during
youth)
Spleen (curves
around left side of
stomach)
Peyer’s patches
(in intestine)
Appendix

 Spleen
 Located on the left side of the abdomen
 Filters and cleans blood of bacteria, viruses, debris
 Provides a site for lymphocyte proliferation and
immune surveillance
 Destroys worn-out blood cells
 Forms blood cells in the fetus
 Acts as a blood reservoir

 Thymus
 Found overlying the heart
 Functions at peak levels only during youth

 Tonsils
 Small masses of lymphoid tissue deep to the mucosa
surrounding the pharynx (throat)
 Trap and remove bacteria and other foreign pathogens
 Tonsillitis results when the tonsils become congested
with bacteria

 Found in the wall of the small intestine
 Similar lymphoid follicles are found in the appendix
 Macrophages capture and destroy bacteria in the
intestine

 Mucosa-associated lymphoid tissue (MALT)

 Includes:
 Tonsils
 Appendix
 Acts as a sentinel to protect respiratory and digestive
tracts

Part II: Body Defenses
 Two mechanisms that make up the immune

system defend us from foreign materials
1. Innate (nonspecific) defense system
2. Adaptive (specific) defense system
 Immunity—specific resistance to disease
 Immune system is a functional system rather than
an organ system in an anatomical sense

Figure 12.6 An overview of the body’s defenses.
The Immune System
Adaptive (specific) defense

Innate (nonspecific) defense mechanisms
mechanisms
First line of defense Second line of defense Third line of defense
• Skin • Phagocytic cells • Lymphocytes

• Mucous membranes • Natural killer cells • Antibodies
• Secretions of skin • Antimicrobial proteins • Macrophages and other
and mucous • The inflammatory antigen-presenting cells
membranes response
• Fever

Body Defenses
 Innate (nonspecific) defense system

 Mechanisms protect against a variety of invaders
 Responds immediately to protect body from foreign
materials
 Adaptive (specific) defense system
 Fights invaders that get past the innate system
 Specific defense is required for each type of invader
 The highly specific resistance to disease is immunity

Innate (Nonspecific) Body Defenses
 Innate body defenses are mechanical barriers to

pathogens (harmful or disease-causing
microorganisms) and include:
 Body surface coverings
 Intact skin
 Mucous membranes
 Specialized human cells
 Chemicals produced by the body
 Table 12.1 provides a more detailed summary

Table 12.1 Summary of Innate (Nonspecific) Body Defenses (1 of 3)



Surface Membrane Barriers
 Surface membrane barriers, such as the skin and

mucous membranes, provide the first line of
defense against the invasion of microorganisms
 Protective secretions produced by these membranes
 Acidic skin secretions inhibit bacterial growth
 Sebum is toxic to bacteria
 Mucus traps microorganisms
 Gastric juices are acidic and kill pathogens
 Saliva and tears contain lysozyme (enzyme that
destroys bacteria)

Internal Defenses: Cells and Chemicals
 Cells and chemicals provide a second line of

defense
 Natural killer cells and phagocytes
 Inflammatory response
 Chemicals that kill pathogens
 Fever

 Natural killer (NK) cells

 Lyse (burst) and kill cancer cells, virus-infected cells
 Release chemicals called perforin and granzymes to
degrade target cell contents

 Inflammatory response
 Triggered when body tissues are injured
 Four most common indicators (cardinal signs) of acute
inflammation
1. Redness
2. Heat
3. Pain
4. Swelling (edema)

Figure 12.7 Flowchart of inflammatory events.
Injurious agents
Cells damaged
Release kinins, histamine,

and other chemicals
Blood vessels Capillaries Neutrophils and then

dilate become “leaky” monocytes
(and other WBCs)
enter area
Increased blood Edema (fluid in Clotting Removal of

flow into area tissue spaces) proteins damaged/dead
enter area tissue cells and
pathogens
from area
Redness Heat Pain Swelling
Brings more
nutrients and Fibrin
oxygen to area barrier
Increases Possible
metabolic temporary
rate of limitation of
tissue cells joint movement
Healing

 Inflammatory response (continued)

 Damaged cells release inflammatory chemicals
 Histamine
 Kinin
 These chemicals cause:
 Blood vessels to dilate
 Capillaries to become leaky
 Phagocytes and white blood cells to move into the area
(called positive chemotaxis)

 Functions of the inflammatory response

 Prevents spread of damaging agents
 Disposes of cell debris and pathogens through
phagocytosis
 Sets the stage for repair

 Process of the inflammatory response

1. Neutrophils migrate to the area of inflammation by
rolling along the vessel wall (following the scent of
chemicals from inflammation)
2. Neutrophils squeeze through the capillary walls by
diapedesis to sites of inflammation
3. Neutrophils gather in the precise site of tissue injury
(positive chemotaxis) and consume any foreign
material present

Figure 12.8 Phagocyte mobilization during inflammation.
3 Positive
chemotaxis
Inflammatory
chemicals diffusing
from the inflamed
site act as chemotactic
agents
Neutrophils
1 Enter blood from bone marrow 2 Diapedesis
and roll along the vessel wall
Capillary wall Endothelium

Basement membrane
 Phagocytes
 Cells such as neutrophils and macrophages engulf
foreign material by phagocytosis
 The phagocytic vesicle is fused with a lysosome, and
enzymes digest the cell’s contents

Figure 12.9a Phagocytosis by a macrophage.
(a) A macrophage (purple) uses its cytoplasmic

extensions to ingest bacillus-shaped
bacteria (pink) by phagocytosis. Scanning
electron micrograph.

Figure 12.9b Phagocytosis by a macrophage. Slide 1
1 Phagocyte
adheres to
pathogens.
2 Phagocyte
Phagosome engulfs the
(phagocytic particles, forming
vesicle) a phagosome.
Lysosome 3 Lysosome
fuses with the
phagocytic vesicle,
forming a
phagolysosome.
Acid
hydrolase 4 Lysosomal
enzymes enzymes digest
the pathogens or
debris, leaving a
residual body.
5 Exocytosis of
the vesicle
removes
indigestible and
(b) Events of phagocytosis residual material.
1 Phagocyte
adheres to
pathogens.
(b) Events of phagocytosis

1 Phagocyte
adheres to
pathogens.
2 Phagocyte

1 Phagocyte
adheres to
pathogens.
2 Phagocyte
Lysosome 3 Lysosome
fuses with the
phagocytic vesicle,
forming a
phagolysosome.
Acid
hydrolase
enzymes

1 Phagocyte
adheres to
pathogens.
2 Phagocyte
Lysosome 3 Lysosome
fuses with the
phagocytic vesicle,
forming a
phagolysosome.
Acid
the pathogens or
debris, leaving a
residual body.

1 Phagocyte
adheres to
pathogens.
2 Phagocyte
Lysosome 3 Lysosome
fuses with the
phagocytic vesicle,
forming a
phagolysosome.
Acid
the pathogens or
debris, leaving a
residual body.
5 Exocytosis of
the vesicle
removes
indigestible and
(b) Events of phagocytosis residual material.
 Antimicrobial proteins
 Enhance innate defenses by:
 Attacking microorganisms directly
 Hindering reproduction of microorganisms
 Most important types
 Complement proteins
 Interferon

 Antimicrobial proteins: complement proteins

 Complement refers to a group of at least 20 plasma
proteins that circulate in the plasma
 Complement is activated when these plasma proteins
encounter and attach to cells (known as complement
fixation)

 Antimicrobial proteins: complement proteins

(continued)
 Membrane attack complexes (MACs), one result of
complement fixation, produce holes or pores in cells
 Pores allow water to rush into the cell
 Cell bursts (lyses)
 Activated complement enhances the inflammatory
response

Figure 12.10 Activation of complement, resulting in lysis of a target cell.
Membrane attack
complex forming
Antibodies
attached to Pore
pathogen’s
membrane
Cytoplasm H2O H2O
1 Activated complement proteins attach to 2 MAC pores in the 3 This influx of water
pathogen’s membrane in step-by-step sequence, membrane allow water causes cell lysis.
forming a membrane attack complex (a MAC attack). to rush into the cell.

 Antimicrobial proteins: interferons

 Interferons are small proteins secreted by virus-
infected cells
 Interferons bind to membrane receptors on healthy cell
surfaces to interfere with the ability of viruses to
multiply

 Fever
 Abnormally high body temperature is a systemic
response to invasion by microorganisms
 Hypothalamus regulates body temperature at 37ºC
(98.6ºF)
 The hypothalamus thermostat can be reset higher by
pyrogens (secreted by white blood cells)
 High temperatures inhibit the release of iron and zinc
(needed by bacteria) from the liver and spleen
 Fever also increases the speed of repair processes

Adaptive Body Defenses
 Adaptive body defenses are the body’s specific

defense system, or the third line of defense
 Immune response is the immune system’s response to
a threat
 Antigens are targeted and destroyed by antibodies

 Three aspects of adaptive defense

 Antigen specific—the adaptive defense system
recognizes and acts against particular foreign
substances
 Systemic—immunity is not restricted to the initial
infection site
 Memory—the adaptive defense system recognizes
and mounts a stronger attack on previously
encountered pathogens

 Two arms of the adaptive defense system

 Humoral immunity = antibody-mediated immunity
 Provided by antibodies present in body fluids
 Cellular immunity = cell-mediated immunity
 Targets virus-infected cells, cancer cells, and cells of
foreign grafts

Antigens
 Antigens are any substance capable of exciting

the immune system and provoking an immune
response
 Examples of common nonself antigens
 Foreign proteins provoke the strongest response
 Nucleic acids
 Large carbohydrates
 Some lipids
 Pollen grains
 Microorganisms (bacteria, fungi, viruses)

Antigens
 Self-antigens
 Human cells have many protein and carbohydrate
molecules
 Self-antigens do not trigger an immune response in us
 The presence of our cells in another person’s body
can trigger an immune response because they are
foreign
 Restricts donors for transplants

Antigens
 Haptens, or incomplete antigens, are not

antigenic by themselves
 When they link up with our own proteins, the immune
system may recognize the combination as foreign and
respond with an attack
 Found in poison ivy, animal dander, detergents, hair
dyes, cosmetics

Cells of the Adaptive Defense System: An
Overview
 Crucial cells of the adaptive system
1. Lymphocytes—respond to specific antigens
 B lymphocytes (B cells) produce antibodies and
oversee humoral immunity
 T lymphocytes (T cells) constitute the cell-mediated arm
of the adaptive defenses; do not make antibodies
2. Antigen-presenting cells (APCs)—help the
lymphocytes but do not respond to specific antigens

Overview
 Lymphocytes
 Arise from hemocytoblasts of bone marrow
 Whether a lymphocyte matures into a B cell or T cell
depends on where it becomes immunocompetent
 Immunocompetence
 The capability to respond to a specific antigen by
binding to it with antigen-specific receptors that appear
on the lymphocyte’s surface

Overview
 Lymphocytes (continued)
 T cells develop immunocompetence in the thymus and
oversee cell-mediated immunity
 Identify foreign antigens
 Those that bind self-antigens are destroyed
 Self-tolerance is important part of lymphocyte
“education”
 B cells develop immunocompetence in bone marrow
and provide humoral immunity

Overview
 Immunocompetent T and B lymphocytes migrate
to the lymph nodes and spleen, where
encounters with antigens occur
 Differentiation from naïve cells into mature
lymphocytes is complete when they bind with
recognized antigens
 Mature lymphocytes (especially T cells) circulate
continuously throughout the body

Figure 12.11 Lymphocyte differentiation and activation. Slide 1
KEY:
Red bone marrow: site of lymphocyte origin
Primary lymphoid organs: sites of
Red development of immunocompetence as
bone marrow B or T cells
Secondary lymphoid organs: sites of
antigen encounter, and activation to
become effector and memory B or T cells
Immature (naive)
lymphocytes 1 Lymphocytes destined to become T cells
migrate (in blood) to the thymus and develop
1 immunocompetence there. B cells develop
immunocompetence in red bone marrow.
Thymus
Bone marrow
2
2 Immunocompetent but still naive
lymphocytes leave the thymus and bone
Lymph nodes, marrow. They “seed” the lymph nodes,
spleen, and other spleen, and other lymphoid tissues, where
lymphoid tissues they encounter their antigens and become
activated.
3 Antigen-activated (mature)
immunocompetent lymphocytes (effector
3 cells and memory cells) circulate
continuously in the bloodstream and lymph
and throughout the lymphoid organs of the
body.

KEY:
Immature (naive)
Thymus
Bone marrow

KEY:
Immature (naive)
Thymus
Bone marrow
2
activated.

KEY:
Immature (naive)
Thymus
Bone marrow
2
activated.
3 Antigen-activated (mature)
immunocompetent lymphocytes (effector
3 cells and memory cells) circulate
continuously in the bloodstream and lymph
and throughout the lymphoid organs of the
body.

Overview
 Antigen-presenting cells (APCs)
 Engulf antigens and then present fragments of them
on their own surfaces, where they can be recognized
by T cells
 Major types of cells behaving as APCs
 Dendritic cells
 Macrophages
 B lymphocytes
 When they present antigens, dendritic cells and
macrophages activate T cells, which release chemicals

Humoral (Antibody-Mediated) Immune
Response
 B lymphocytes with specific receptors bind to a
specific antigen
 The binding event sensitizes, or activates, the
lymphocyte to undergo clonal selection
 A large number of clones is produced (primary
humoral response)

Response
 Most of the B cell clone members (descendants)
become plasma cells
 Produce antibodies to destroy antigens
 Activity lasts for 4 or 5 days
 Plasma cells begin to die
 Some B cells become long-lived memory cells
capable of mounting a rapid attack against the
same antigen in subsequent meetings (secondary
humoral response)
 These cells provide immunological memory

Figure 12.12 Clonal selection of a B cell.
Primary response Free antigen

(initial encounter Antigen binding
with antigen) to a receptor on a
specific B cell
(B cells with
Proliferation to non-complementary
form a clone receptors remain
Activated B
inactive)
cells
Plasma Memory
cells B cell
Secreted
antibody
molecules
Secondary response Subsequent

challenge
(can be years later)
by same
Clone of cells antigen results
identical to in more rapid
ancestral cells response
Plasma
cells
Secreted
Memory
antibody
B cells
molecules
Figure 12.13 Primary and secondary humoral responses to an antigen.
Relative antibody concentration

Secondary
response
Primary
in blood plasma
response
0 1 2 3 4 5 6
Time (weeks)
Antigen Antigen
injected injected
Response
 Active immunity
 Occurs when B cells encounter antigens and produce
antibodies
 Active immunity can be:
 Naturally acquired during bacterial and viral infections
 Artificially acquired from vaccines

Response
 Passive immunity
 Occurs when antibodies are obtained from someone
else
 Naturally acquired from a mother to her fetus or in the
breast milk
 Artificially acquired from immune serum or gamma
globulin (donated antibodies)
 Immunological memory does not occur
 Protection is short-lived (2–3 weeks)

Response
 Passive immunity (continued)
 Monoclonal antibodies
 Antibodies prepared for clinical testing for diagnostic
services
 Produced from descendants of a single cell line
 Exhibit specificity for only one antigen
 Examples of uses for monoclonal antibodies
 Cancer treatment
 Diagnosis of pregnancy
 Treatment after exposure to hepatitis and rabies

Figure 12.14 Types of humoral immunity.
Humoral
immunity
Active Passive
Naturally Artificially Naturally Artificially

acquired acquired acquired acquired
Infection; Vaccine; Antibodies Injection of
contact with dead or passed from donated
pathogen attenuated mother to antibodies
pathogens fetus via (gamma
placenta; or globulin)
to infant in
her milk
Response
 Antibodies (immunoglobulins, Igs)
 Constitute gamma globulin part of blood proteins
 Soluble proteins secreted by activated B cells (plasma
cells)
 Formed in response to a huge number of antigens

Figure 12.15a Basic antibody structure.
(a)

Response
 Antibody structure
 Four polypeptide chains, two heavy and two light,
linked by disulfide bonds to form a T- or Y-shaped
molecule
 Each polypeptide chain has a variable (V) region and a
constant (C) region
 Variable regions form antigen-binding sites, one on
each arm of the T or Y
 Constant regions determine the type of antibody formed
(antibody class)

Figure 12.15b Basic antibody structure.
Antigen-binding
sites
Light
chain
Disulfide Heavy
bonds C C chain
(b)
Response
 Antibody classes
 Antibodies of each class have slightly different roles
and differ structurally and functionally
 Five major immunoglobulin classes (MADGE)
1. IgM—can fix complement
2. IgA—found mainly in secretions, such as mucus or
tears
3. IgD—important in activation of B cell
4. IgG—can cross the placental barrier and fix
complement; most abundant antibody in plasma
5. IgE—involved in allergies

Table 12.2 Immunoglobulin Classes (1 of 2)

Table 12.2 Immunoglobulin Classes (2 of 2)

Response
 Antibody function
 Antibodies inactivate antigens in a number of ways
 Complement fixation: chief antibody ammunition used
against cellular antigens
 Neutralization: antibodies bind to specific sites on
bacterial exotoxins or on viruses that can cause cell
injury
 Agglutination: antibody-antigen reaction that causes
clumping of cells
 Precipitation: cross-linking reaction in which antigen-
antibody complex settles out of solution

Figure 12.16 Mechanisms of antibody action.
Antigen Antigen-antibody Antibody

complex
Inactivates by Fixes and activates
Neutralization
Agglutination Precipitation
(masks dangerous
(cell-bound (soluble Complement
parts of bacterial
antigens) antigens)
exotoxins; viruses)
Enhances Enhances Leads to
Phagocytosis Inflammation Cell lysis
Chemo-
taxis
Histamine
release
Cellular (Cell-Mediated) Immune Response
 Main difference between two arms of the adaptive

response
 B cells secrete antibodies
 T cells fight antigens directly

 Like B cells, immunocompetent T cells are

activated to form a clone by binding with a
recognized antigen
 Unlike B cells, T cells are unable to bind to free
antigens
 Antigens must be presented by a macrophage, and
double recognition must occur
 APC engulfs and presents the processed antigen in
combination with a protein from the APC

 Different classes of effector T cells

 Helper T cells
 Cytotoxic T cells
 T cells must recognize nonself and self through
the process of antigen presentation
 Nonself—the antigen fragment presented by APC
 Self—coupling with a specific glycoprotein on the
APC’s surface at the same time

Figure 12.17 T cell activation and interactions with other cells of the immune response.
Antigen “Presented” Cell-mediated

Cytotoxic
antigen immunity
(killer)
T cell antigen T cell (attack on
receptor infected cells)
Dendritic cell Helper

T cell
Cytokines
Humoral
Self- immunity
Antigen protein (secretion of
B cell
processing antibodies by
Cytokines
plasma cells)

 Cytotoxic (killer) T cells

 Specialize in killing infected cells
 Insert a toxic chemical (perforin or granzyme)
 The perforin enters the foreign cell’s plasma
membrane
 Pores now appear in the target cell’s membrane
 Granzymes (protein-digesting enzymes) enter and kill
the foreign cell
 Cytotoxic T cell detaches and seeks other targets

Figure 12.18 A proposed mechanism by which cytotoxic T cells kill target cells. Slide 1
Cytotoxic
T cell 1
Cytotoxic T cell 2 Cytotoxic T cell
binds tightly to the releases perforin and
foreign target cell. granzyme molecules from
its granules by exocytosis.
Perforin Granule 3 Perforin molecules
insert into the target
cell membrane and
TC cell form pores similar to
membrane those produced by
complement activation.
Target
cell 4 Granzymes enter
membrane the target cell via the
Target Perforin pores and degrade
cell pore cellular contents.
Granzymes
5 The cytotoxic T cell detaches

and searches for another prey.

Cytotoxic
T cell 1
Cytotoxic T cell
binds tightly to the
foreign target cell.
Target
cell

Cytotoxic
T cell 1
Perforin Granule
TC cell
membrane
Target
cell
membrane
Target
cell

Cytotoxic
T cell 1
cell membrane and
Target
cell
membrane
Target Perforin
cell pore

Cytotoxic
T cell 1
cell membrane and
Target
Granzymes

Cytotoxic
T cell 1
cell membrane and
Target
Granzymes
5 The cytotoxic T cell detaches

and searches for another prey.

 Helper T cells
 Recruit other cells to fight invaders
 Interact directly with B cells bound to an antigen,
prodding the B cells into clone production
 Release cytokines, chemicals that act directly to rid the
body of antigens

 Regulatory T cells
 Release chemicals to suppress the activity of T and B
cells
 Stop the immune response to prevent uncontrolled
activity
 A few members of each clone are memory cells
 A summary of cells and molecules follows
(Figure 12.19)

Figure 12.19 A summary of the adaptive immune responses.
HUMORAL (ANTIBODY-MEDIATED) ADAPTIVE CELLULAR (CELL-MEDIATED) ADAPTIVE

IMMUNE RESPONSE IMMUNE RESPONSE
Antigen (1st exposure)
Engulfed by
Macrophage
Free antigens Antigens displayed by
directly activate Becomes infected cells activate
Antigen-
presenting
cell
Presents antigen Cytotoxic
Stimulates T cell
Stimulates Helper Stimulates

B cell
T cell
Memory
T cell
Gives rise to Stimulates Stimulates Stimulates Gives rise to
Antigen (2nd exposure) Active

cytotoxic
Stimulates T cells
Plasma
cells
Secrete Memory Memory

B cells T cells
Antibodies
Defend against extracellular pathogens by Defend against intracellular pathogens and

binding to antigens and making them easier cancer by binding to and lysing the infected
targets for phagocytes and complement. cells or cancer cells.

Table 12.3 Functions of Cells and Molecules Involved in Immunity (1 of 4)




Organ Transplants and Rejection
 Major types of transplants, or grafts

 Autografts—tissue transplanted from one site to
another on the same person
 Isografts—tissue grafts from a genetically identical
person (identical twin)
 Allografts—tissue taken from a person other than an
identical twin (most common type of graft)
 Xenografts—tissue taken from a different animal
species (never successful)

Organ Transplants and Rejection
 Blood group and tissue matching is done to

ensure the best match possible
 75% match is needed to attempt a graft
 Organ transplant is followed by
immunosuppressive therapy to prevent rejection

Disorders of Immunity
 The most important disorders of the immune

system
 Allergies
 Autoimmune diseases
 Immunodeficiencies

 Allergies
 Allergies, or hypersensitives, are abnormal, vigorous
immune responses
 The immune system overreacts to an otherwise
harmless antigen, and tissue damage occurs

 Types of allergies
 Immediate (acute) hypersensitivity
 Seen in hives and anaphylaxis
 Due to IgE antibodies and histamine
 Anaphylactic shock is systemic, acute allergic response
and is rare
 Delayed hypersensitivity
 Reflects activity of T cells, macrophages, and cytokines
 Symptoms usually appear 1–3 days after contact with
antigen
 Allergic contact dermatitis (poison ivy, cosmetics)

Homeostatic Imbalance 12.4 Mechanism of an immediate (acute) hypersensitivity response. Slide 1
Sensitization stage
1 Antigen (allergen) invades body.
2 Plasma cells produce large

amounts of class IgE antibodies
against allergen.
Mast cell with fixed IgE
3 IgE antibodies attach to mast antibodies
cells in body tissues (and to
IgE
circulating basophils).
Granules containing
histamine
Subsequent (secondary)
responses
4 More of same allergen Antigen
invades body. Mast cell granules
release contents after
5 Allergen binding to IgE
antigen binds with IgE
on mast cells triggers release of antibodies
histamine (and other chemicals).
Histamine
6 Histamine causes blood vessels to dilate and become leaky, which

promotes edema; stimulates release of large amounts of mucus;
and causes smooth muscles to contract.
Outpouring Release of Constriction of

of fluid from mucus bronchioles
capillaries
Sensitization stage

Sensitization stage

against allergen.

Sensitization stage

against allergen.
circulating basophils). IgE
Granules containing
histamine

responses
invades body.

responses
invades body.
Mast cell granules
5 Allergen binding to IgE release contents after
on mast cells triggers release of antigen binds with IgE
histamine (and other chemicals). antibodies
Histamine

responses
invades body.
Mast cell granules
5 Allergen binding to IgE release contents after
on mast cells triggers release of antigen binds with IgE
histamine (and other chemicals). antibodies
Histamine


capillaries
Sensitization stage

against allergen.
IgE
circulating basophils).
Granules containing
histamine
responses
invades body. Mast cell granules
release contents after
5 Allergen binding to IgE
antigen binds with IgE
on mast cells triggers release of antibodies
histamine (and other chemicals).
Histamine


capillaries
 Autoimmune diseases
 Occurs when the body’s self-tolerance breaks down
 The body produces auto-antibodies and sensitized T
lymphocytes that attack its own tissues
 Most forms of autoimmune disease result from the
appearance of formerly hidden self-antigens or
changes in the structure of self-antigens, and
antibodies formed against foreign antigens that
resemble self-antigens

 Examples of autoimmune diseases

 Rheumatoid arthritis—destroys joints
 Myasthenia gravis—impairs communication between
nerves and skeletal muscles
 Multiple sclerosis—white matter of brain and spinal
cord is destroyed
 Graves’ disease—thyroid gland produces excess
thyroxine

 Examples of autoimmune diseases (continued)

 Type I diabetes mellitus—destroys pancreatic beta
cells, resulting in deficient insulin production
 Systemic lupus erythematosus (SLE)—affects kidney,
heart, lung, and skin
 Glomerulonephritis—severe impairment of kidney
function due to acute inflammation

Autoimmune Disease
 Immunodeficiencies
 May be congenital or acquired
 Severe combined immunodeficiency disease (SCID) is
a congenital disease
 AIDS (acquired immune deficiency syndrome) is caused
by a virus that attacks and cripples the helper T cells
 Result from abnormalities in any immune element
 Production or function of immune cells or complement
is abnormal

Part III: Developmental Aspects of the
Lymphatic System and Body Defenses
 Lymphatic vessels form by budding off from veins
 Lymph nodes present by fifth week of
development
 The thymus and the spleen are the first lymphoid
organs to appear in the embryo
 Other lymphoid organs are poorly developed
before birth
 The immune response develops around the time
of birth

Part III: Developmental Aspects of the
Lymphatic System and Body Defenses
 The ability of immunocompetent cells to recognize
foreign antigens is genetically determined
 Stress appears to interfere with normal immune
response
 Efficiency of immune response wanes in old age,
and infections, cancer, immunodeficiencies, and
autoimmune diseases become more prevalent

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Chapter 12

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 Consists of two semi-independent parts:

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 Lymph consists of excess tissue fluid and plasma

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Blood Loose connective

 Lymphatic vessels (lymphatics)

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(a) Arteriole Venule

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 Lymphatic collecting vessels

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Cervical Internal jugular vein

 Lymphatic vessels are similar to veins of the

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 Lymph nodes filter lymph before it is returned to

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 Defense cells within lymph nodes

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 Most lymph nodes are kidney-shaped, less than

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 Flow of lymph through nodes

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 Several other lymphoid organs contribute to

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Thymus (in thorax;

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 Mucosa-associated lymphoid tissue (MALT)

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 Two mechanisms that make up the immune

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The Immune System

Adaptive (specific) defense

First line of defense Second line of defense Third line of defense

• Skin • Phagocytic cells • Lymphocytes

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 Innate (nonspecific) defense system

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 Innate body defenses are mechanical barriers to

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 Surface membrane barriers, such as the skin and

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 Cells and chemicals provide a second line of

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 Natural killer (NK) cells

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Release kinins, histamine,

Blood vessels Capillaries Neutrophils and then

Increased blood Edema (fluid in Clotting Removal of

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 Inflammatory response (continued)

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