CHAPTER 21

The Lymphatic and Immune System

Chapter Objectives:
After studying this chapter, you will be able to:
• Identify the components and anatomy of the lymphatic system
• Discuss the role of the innate immune response against pathogens
• Describe the power of the adaptive immune response to cure disease
• Explain immunological deficiencies and over-reactions of the immune system
• Discuss the role of the immune response in transplantation and cancer
• Describe the interaction of the immune and lymphatic systems with other body systems

21.1 Anatomy of the Lymphatic and Immune Systems

Functions of the Lymphatic System
a. Collects and transports excess fluids and returns them to the bloodstream
b. Filters pathogens from the blood and lymph
c. Transports dietary lipids and fat-soluble vitamins absorbed by digestive
system
2. Structure of the Lymphatic System
a. Lymph is not actively pumped by the heart; forced through vessels by
skeletal muscle contraction and breathing
b. One-way valves prevent backflow
i. Lymphatic Capillaries – also, terminal lymphatics = blind-end
vessels located in all body tissues except CNS, bones and marrow,
teeth, and cornea of eye
1. one-cell thick endothelium with overlapping cells acting as
flaps
2. increased interstitial pressure forces fluid in; flaps prevent
outflow
3. lacteals – specialized lymph vessels in small intestine
transport chyle (milky, lipid-rich lymph) to bloodstream
ii. Larger Lymphatic Vessels, Trunks, and Ducts
1. Lymphatic capillaries empty into larger lymphatic vessels;
three-tunic structure (similar to veins) with valves that create
a beaded appearance
2. Superficial and deep lymphatic vessels empty into lymphatic
trunks, which in turn empty into lymphatic ducts
 a. Right lymphatic duct – drains lymph from right side of
head, thorax, and right upper limb into right subclavian
vein
b. Thoracic duct – drains rest of the body into left
subclavian vein
i. Begins at cisterna chyli – sac-like chamber
collecting lymph from lower body and abdomen
through right, left, and intestinal trunks
ii. Other lymphatic vessels join thoracic duct above
the cisterna chyli before draining into left
subclavian vein

Fig. 21.4 Major Trunks and

Ducts of the Lymphatic System

3. The Organization of Immune Function

a. Three phases based on timing of effects: barrier defenses, innate immune
response, and adaptive immune response
i. Barrier defenses, ex. skin and mucous membranes, act
instantaneously to prevent pathogens from entering the body
ii. Innate response – rapid and non-specific response by specialized
cells and soluble factors (chemical responses)
 iii. Adaptive response – slower response, but specific to pathogen;
primarily controlled by lymphocytes

4. Lymphocytes: B Cells, T Cells, Plasma Cells, and Natural Killer Cells

a. The body contains ~1012 lymphocytes; circulating in blood and lymph and
residing within secondary lymphoid organs such as the lymph nodes, spleen,
tonsils, thymus
b. B cells - When stimulated by antigen, B cells differentiate into plasma cells,
which produce and secrete antibodies
i. Antigen = chemical structure on surface of pathogen the binds to T
cell or B cell receptor and elicits immune response
ii. Antibodies = proteins that bind specifically to antigens
c. T cells - T cells are diverse and provide cell-mediated immunity (discussed
later)
d. Plasma cells - differentiated B cells which secrete soluble antibodies
e. Natural killer (NK) cells – part of non-specific innate response; contains
cytotoxic (cell-killing) granules and are first-line defense against viruses and
certain cancers
5. Primary Lymphoid Organs and Lymphocyte Development
a. B and T cells mature, proliferate, and undergo selection in bone marrow and
thymus; this process trains the adaptive immune cells to recognize self and
non-self and destroy only pathogens
b. Bone marrow – red bone marrow is site of hematopoiesis (blood cell
differentiation)
i. B cells complete maturation here; T cells form here, but leave as
immature cells (thymocytes) and complete maturation in thymus
c. Thymus – bilobed glandular organ located between sternum and aorta;
surrounded by a connective tissue capsule that divides it into left and right
lobes, which are further divided into lobules by trabeculae
i. Each lobule consists of a dark-staining outer cortex and a lighter
central medulla
ii. Thymic involution (shrinking of thymus gland) may contribute to
immunosenescence (age-related loss of immune function)
6. Secondary Lymphoid Organs and their Roles in Active Immune
Responses
a. Naïve lymphocytes (fully mature T and B cells that have not yet
encountered a pathogen) circulate in bloodstream and concentrate in
secondary lymphoid organs
b. Lymph nodes, spleen, and lymphoid nodules share common features:
i. Internal structure of reticular fibers with attached macrophages
ii. Lymphoid follicles – containing germinal centers; B cell and T cell
rich areas where rapid proliferation occurs
iii. High endothelial venules – structure allows blood cells to enter
lymphoid tissues directly
 1. Lymph nodes - small bean-shaped lymphoid organs; located in the cervical
region, axillary region, and inguinal region. As lymph flows through a lymph
node, dendritic cells and macrophages remove most pathogens; adaptive
immune response is stimulated as needed.
a. The path of lymph flow through a lymph node is as follows:
i. Afferent lymphatic vessels – transport lymph into the
lymph node from the peripheral tissues; afferent
lymphatic vessels penetrate the capsule of the lymph
node on the side opposite the hilum (a shallow
depression where the blood vessels and nerves enter
and leave the organ)
ii. Afferent vessels deliver the lymph to the subcapsular
space, a meshwork of reticular fibers, macrophages,
and dendritic cells
iii. Lymph next flows in the outer cortex which contains B
cells within germinal centers
iv. Lymph then flows through the lymph sinuses to the
deep cortex which is dominated by T cells
v. Lymph continues into the medullary sinuses which
contain B cells and plasma cells.
vi. Efferent lymphatic vessels – drain lymph out of the
lymph node at the hilum
2. Spleen - largest lymphoid organ (~12 cm long); removes abnormal red
blood cells, stores iron from recycled RBCs, and initiates immune response
by B cells and T cells to antigens in the bloodstream
a. attached to lateral border of the stomach by the gastrosplenic
ligament
b. surrounded by a delicate capsule; fragile and highly vascularized;
easily damaged and difficult to repair; often removed by splenectomy
c. Fibrous trabeculae radiate outward toward the capsule through the
interior from the hilum; blood vessels travel within the trabeculae to
splenic nodules containing red pulp and white pulp
d. Red pulp contains large quantities of red blood cells; white pulp
resembles lymphoid nodules and contains lymphocytes
3. Lymphoid Nodules – areas of densely packed lymph tissue or lymphocytes; no
distinct boundaries because they lack fibrous capsule
a. Tonsils - large lymphoid nodules in the walls of the pharynx; tonsillar
crypts formed by invagination of epithelial tissue collect materials taken in
through breathing and eating; encourage pathogens to collect for
subsequent elimination
b. MALT (Mucosa-associated lymphoid tissue) - aggregate of lymphoid
follicles directly associated with mucous membranes; found underlying
the mucosa of the gastrointestinal tract, breast tissue, lungs, and eyes
i. Peyer’s patches – aggregates of MALT located in small intestine that
protect against pathogens in ingested substances; infection or
inflammation can lead to appendicitis
 c. BALT (Bronchial-associated lymphoid tissue) – located along bronchi
and between bronchi and arteries; protects against inhaled pathogens

21.2 Barrier Defenses and the Innate Immune Response

1. Innate Immunity – Physical barriers

2. Cells of the Innate Immune Response

a. Phagocytes: Macrophages and Neutrophils
i. Phagocytes = cells that engulf old cells, pathogens, or debris; process
is phagocytosis
ii. Phagocyte engulfs cells or debris in phagosome which fuses with
lysosome and is broken down with digestive enzymes
iii. Major phagocytes are macrophages, neutrophils, and dendritic
cells
1. Macrophages – amoeboid cells that move through tissues and
squeeze through capillary walls using pseudopodia
a. Most versatile phagocyte
b. Can be free-roaming or fixed to reticular fibers in
specific organs; ex. Kupffer cells in liver and alveolar
macrophages in lungs
2. Neutrophils – attracted to infected tissue via chemical signals
a. Are granulocytes - contain cytoplasmic granules that
become vasoactive mediators, like histamine
b. Primary pathogen-killer of the innate response
3. Monocytes – precursor cells that can differentiate into
macrophages or dendritic cells
 b. Natural Killer (NK) cells – induce apoptosis (programmed cell death) in
infected cells via two different mechanisms:
i. Fas ligand – suface molecule that binds to fas receptor on infected cell
and sends signals to induce apoptosis
ii. Perforins and granzymes – perforins form pores in cell membrane of
infected cells; granzymes enter through pores and trigger apoptosis
intracellularly
3. Recognition of Pathogens
a. Pattern recognition receptor (PRR) – membrane-bound receptor on cells
of innate response that recognize patterns of pathogen-specific molecules
and molecules released by stressed or damaged cells
4. Soluble Mediators of the Innate Immune Response
a. Cytokines and Chemokines – soluble chemical mediators
i. Cytokines = signaling molecule secreted into intracellular space;
communicates over short distances; causes physiological change in
receiving cells
ii. Chemokines = similar to cytokines but effective over longer distances
b. Early Induced Proteins – not constitutively present, but produced early in
innate response
i. Interferons = EAPs secreted by virus-infected cells; induce adjacent
cells to produce anti-viral proteins
ii. Mannose-binding protein and C-reactive protein bind to bacterial
cell walls; phagocytes recognize these EAPs and are attracted to
bacterial cells; opsonization – process of tagging a pathogen for
phagocytosis
c. Complement System – series of proteins produced by the liver that is found
constitutively in blood plasma
i. Functions in innate response via the “alternate pathway” and in the
adaptive response via the “classical pathway”
ii. Consists of series of proteins that enzymatically alter proteins later in
the series; often described as a cascade
iii. Once activated, the cascade is irreversible and leads to production of
fragments that:
1. Bind to pathogen cell membrane to label them for opsonization
2. Act as chemotactic agents to attract phagocytes
3. Form pores in pathogen cell membrane
iv. See Figure 21.13 for steps of the complement cascade
5. Inflammation Response
a. Inflammation – “hallmark” of innate immune response to tissue damage due
to infection or injury; four characteristics: heat, redness, pain, swelling
i. Damage cells release contents, which triggers inflammatory response
and brings phagocytic and other innate immune cells to the damaged
area
ii. Brings cells and fluids to kill pathogens and clear debris; also limits
spread by isolating the site
 iii. Inflammation can be acute (short-term) or chronic (long-term)
iv. Four parts of the inflammatory response are:
1. Tissue injury – contents released from damaged cells
stimulate release of mast cell granules containing soluble
mediators, ex. histamine, leukotrienes, and prostaglandins
a. Histamine causes vasodilation and increases vascular
permeability
b. Leukotrienes attract neutrophils and increase vascular
permeability
c. Prostaglandins trigger pain
2. Vasodilation – increased blood flow to site; responsible for
heat and redness
3. Increased Vascular Permeability - plasma leaks into
interstitial space and causes swelling (edema)
4. Recruitment of Phagocytes – neutrophils and macrophages
are attracted to site to destroy pathogens and clean up debris;
large numbers of neutrophils die and cellular remains are pus
b. Advantages of Inflammation
i. Pathogens killed and debris removed
ii. Increased permeability encourages entry of clotting factors which
initiate wound repair
iii. Facilitates transport of antigen to lymph nodes by dendritic cells
which develops the adaptive immune response

21.3 The Adaptive Immune Response: T Lymphocytes and Their

Functional Types

1. Benefits of the Adaptive Immune Response – greatest strength is specificity

a. Primary Disease and Immunological Memory
i. Primary adaptive response = first exposure to a pathogen
1. Symptoms may be severe as response takes time
ii. Secondary adaptive response = stronger and faster; often
eliminates pathogen before symptoms are apparent
1. Basis of immunological memory – protects from repeat
infection by the same pathogen
2. Early exposure protects from disease later in life
b. Self-Recognition – distinguish between self-antigens and foreign antigens
i. T and B cell maturation trains them to tolerate self-antigens;
breakdowns in these mechanisms leads to autoimmune disease
(discussed later)
2. T Cell-Mediated Immune Responses
a. Directly control multiple immune responses (cell-mediated immunity)
b. Also often control responses of B cells
 c. Recognize antigens via two-chain protein receptor; variable region domain
determines specificity of antigen recognition; each T cell is specific to a single
antigen
3. Antigens – protein or carbohydrate markers on pathogen cell membranes
consisting of multiple antigenic determinants (epitopes), or regions of antigens
where receptors can bind
a. Antigen Processing and Presentation
i. T-cells cannot recognize antigen directly; antigens must be processed
and presented to the T cell by specialized Antigen Presenting Cells
(APCs) or infected body cells
ii. Antigen processing – mechanism that enzymatically cleaves antigen
into smaller pieces
iii. Antigen presentation – occurs when fragments of antigens are
associated with major histocompatibility complex molecules
(MHCs), glycoproteins on the surface of APCs or body cells
iv. Two classes of MHCs:
1. Class I MHCs– found on every body cell to allow body cells
infected with virus to alert the immune system that they’ve
been attacked by infection and reveal the identity of their
attacker
2. Class II MHCs – found only on the membranes of APCs
(macrophages, neutrophils or eosinophils, and dendritic cells)
a. Class II MHCs allow APCs to alert the body that infection
has been discovered and stimulate other immune
system cells to rush to the site of infection to help with
the attack
b. Professional Antigen-presenting Cells
i. Macrophages, dendritic cells, and B cells are “professional” APCs
because they affect other arms of the immune response
1. Macrophages stimulate T cells to release cytokines
2. Dendritic cells bring antigens to regional lymph nodes
3. B cells present antigens to T cells; necessary to trigger certain
types of antibody responses
4. T Cell Development and Differentiation
a. T cell tolerance = process of eliminating T cells that might attack one’s own
body tissues; T cell tolerance occurs in thymus
b. Double-negative thymocytes lack both CD4 and CD8 molecules
i. Step 1: Untrained (double-negative, --) thymocytes from bone
marrow enter thymic cortex
ii. Step 2: Positive selection - thymic epithelial cells present MHC
proteins to untrained thymocytes; those that bind with MHCs
continue, and those that cannot bind undergo apoptosis
iii. Step 3: Surviving thymocytes receive both CD4 and CD8 receptors,
becoming double-positive (++)
 iv. Step 4: Negative selection (selection for thymocytes that won’t bind) –
double-positive thymocytes move to thymic medulla where they
encounter APCs presenting self-antigens; thymocytes that bind to self-
antigens undergo apoptosis, as this indicates they will attack body
cells
v. Step 5: Cell signals cause self-tolerant thymocytes to express either
CD4 or CD8 receptors, but not both; those expressing CD4s become
helper T cells and those expressing CD8s become cytotoxic T cells

5. Mechanisms of T Cell-mediated Immune Responses

a. Clonal Selection and Expansion
i. Clones are lymphocytes that share the same antigen receptor
ii. Clonal expansion = proliferation of T cells through mitosis; triggered
by recognition of foreign antigen associated with self-MHC molecule
 iii. Clonal selection = process of antigen binding only to T cells with
receptors specific to that antigen
iv. Result of clonal selection and expansion is large numbers of
lymphocytes available to fight a specific pathogen
6. The Cellular Basis of Immunological Memory
a. During primary adaptive immune response both memory T cells and
effector T cells are generated
b. Memory T cells are long-lived and can generate a rapid secondary adaptive
response leading to generation of large numbers of effector T cells quickly
enough to overwhelm pathogen before it causes disease symptoms =
immunity
7. T Cell Types and their Functions
a. CD4 and CD8 are cell adhesion molecules that bind to MHCs on APCs and
keep T cells in close contact with the APC
b. T cells are also held close to APC through binding of receptor to antigen itself
c. CD4 is associated with helper T cells and CD8 is associated with cytotoxic T
cells
d. Helper T Cells (TH or Th) and their Cytokines
i. Th1 cells secrete cytokines that regulate immunological activity of a
variety of cells, including macrophages and other types of T cells
ii. Th2 cells secrete cytokines that act on B cells to drive their
differentiation into plasma cells
e. Cytotoxic T Cells (TC or Tc) kill target cells by inducing apoptosis
i. Tc cells use same mechanism as NK cells (Fas ligand or perforins and
granzymes)
ii. Especially important in anti-viral response
f. Regulatory T Cells (TR or Treg), also suppressor T cells, suppress other T
cell responses to keep them from becoming overreactive

21.4 The Adaptive Immune Response: B-lymphocytes and

Antibodies
1. Antibodies, also immunoglobulins = secreted form of B cell receptor proteins that
bind to specific antigens and cause agglutination (clumping)
a. Five classes of antibody in humans: IgM, IgD, IgG, IgA, and IgE
b. Antibodies can bind to antigens without association with MHCs or APCs
2. B Cell Differentiation and Activation
a. B cells differentiate and mature in bone marrow; up to 100 trillion different
clones of B cells are generated (similar diversity to T cell clones)
b. Central tolerance – process by which B cells that recognize and bind self-
antigens are destroyed or inactivated
i. Clonal deletion = immature B cells that bind to self-antigens on
tissues are signaled to induce apoptosis
 ii. Clonal anergy = B cells exposed to soluble antigen in bone marrow
are not destroyed but become unable to function
c. Peripheral tolerance is T cell-controlled; naïve B cells bind to self-antigen
but do not receive the required signal from a helper T cell to begin making
antibody; signaled to initiate apoptosis
3. Antibody Structure
a. Four-chain Models of Antibody Structures
i. An antibody molecule consists of four polypeptide chains: one pair of
heavy chains on the interior and one pair of light chains on the
exterior
ii. Fc region formed by the two heavy chains – usually linked by
disulfide bonds; Fc region can bind with receptors on other immune
cells, allowing them to specifically bind with antibody-coated
pathogens
iii. Each of the four chains has a constant region where the amino acid
sequence is the same and a variable region where the amino acid
sequence is unique
iv. Variable region amino acid sequence determines shape of antigen-
binding site which determines specificity to pathogen
b. Five Classes of Antibodies and their Functions -classes are determined by
differences in the structure of the heavy-chain constant regions and so have
no effect on the antibody’s specificity
1. IgA – a dimer found primarily in glandular secretions such as
mucus, tears, saliva, breast milk, sweat, and semen; attack the
pathogens before they gain access to internal tissues
2. IgD – a monomer found on the surface of B-cells where it can bind
antigens in the extracellular fluids; binding plays a role in the
sensitization of the B cell so that it proliferates to form the clone
army
3. IgE – a monomer that attaches as an individual molecule to the
exposed surfaces of basophils and mast cells which initiate the
inflammatory response via histamine and heparin
4. IgG – account for 80% of all antibodies; responsible for resistance
against many viruses, bacteria, and bacterial toxins; IgG are
monomers and can cross the placenta
5. IgM – a pentamer secreted after an antigen is encountered; anti-A
and anti-B antibodies responsible for the agglutination of the
incompatible blood types are IgM antibodies
4. Clonal Selection of B Cells
a. Similar to clonal selection of T cells; B cells with antigen specificity are
selected for and expanded; some eventually differentiate into plasma cells
which secrete soluble antibodies with identical specificity to surface antigen
receptors of selected B cells
5. Primary versus Secondary B Cell Responses
a. Similar process to T cells; primary response is slower; secondary response is
more rapid and produces higher levels of antibodies
 b. Secondary response can overwhelm pathogens quickly, often before
symptoms are felt - immunity
6. Active versus Passive Immunity
a. Active – resistance to a pathogen is acquired during an adaptive immune
response within an individual
i. Natural active immunity – acquired by infection with a pathogen
ii. Artificial active immunity – acquired through vaccination
b. Passive – transfer of antibodies to an individual without requiring their own
adaptive immune response
i. Natural passive immunity – during fetal development, IgG is passed
from maternal circulation to fetus via the placenta; after birth, a
newborn gets IgA from breast milk
ii. Artificial passive immunity – usually involves injection of antibodies
from another animal previously exposed to a pathogen
iii. Both natural and artificial passive immunity are temporary and do not
lead to immunological memory
7. T cell-dependent versus T cell-independent Antigens
a. T cell-dependent antigen – B cell requires T cell activation to secrete
antibodies
b. T cell-independent antigen – B cell does not require T cell activation

21.5 The Immune Response against Pathogens

1. Seroconversion – reciprocal relationship between virus levels and antibody levels
in the blood
a. As antibody levels rise, viral load declines
b. May or may not be sufficient to clear a virus completely, ex. HIV
2. The Mucosal Immune Response – IgA and IgM in mucous secretions can neutralize
some pathogens
a. Neutralization = coating a pathogen with antibodies making it incapable of
binding to host cell receptors
3. Defenses against Bacteria and Fungi
a. Macrophage oxidative metabolism – special metabolic pathway used to kill
bacteria (like Mycobacterium) that can survive inside macrophages
4. Defenses against Parasites
a. Parasites, especially worms, used to be much more common and drove the
evolution of the mucosal immune response, IgE-mediated allergies and
asthma, and eosinophils
5. Defenses against Viruses
a. Primary anti-viral defenses are NK cells, cytotoxic T cells, and interferons
6. Evasion of the Immune System by Pathogens
a. Pathogens and hosts have co-evolved so pathogens have evolved ways to
evade the immune response
 b. Bacteria and viruses can mutate; different strains or variants can be more
difficult to treat or prevent
c. Genetic recombination can occur when two viruses infect the same cell; ex.
2010 H1N1 swine flu
d. Pathogens can produce immunosuppressive molecules

21.6 Diseases Associated with Depressed or Overactive Immune

Responses
1. Immunodeficiencies
a. Inherited Immunodeficiencies
i. Severe combined immunodeficiency (SCID) syndrome is a
congenital condition that results from a genetic disorder leading to
deficits in both B and T cells
b. Human Immunodeficiency Virus (HIV)/ AIDS
i. Acquired immune deficiency syndrome (AIDS) is caused by the
Human immunodeficiency virus (HIV) is a condition that destroys the
helper T cells thus depressing cell-mediated immunity; most patients
die of opportunistic infections such as the flu or pneumonia
2. Hypersensitivities - Allergies occur when the antibody response is so severe it
causes tissue damage as it fights off a perceived infection, or allergen, that would
otherwise be harmless to the body (such as pollen or pet dander)
a. Immediate hypersensitivity (Type I) = begins within seconds of exposure
and lasts half to one hour; ex. anaphylactic shock and allergic rhinitis
b. Subacute hypersensitivity (Type II – III) =onset is 1-3 hours after exposure
and the duration is 10-15 hours; ex. Type II = transfusion of mismatched
blood and Type III = farmer’s lung
c. Delayed hypersensitivity (Type IV) = occurs within 1-3 days and lasts for a
week or more; ex. contact dermatitis such as poison ivy and the tuberculosis
skin test
3. Autoimmune Responses
a. Occur when B cells make antibodies (autoantibodies) against normal body
tissues
b. Some examples of autoimmune diseases:
i. Multiple sclerosis – autoantibodies attack white matter of the
nervous system leading to demyelination of neurons which can
cause weakness or even paralysis.
ii. Rheumatoid arthritis – autoantibodies destroy the connective
tissues associated with joints or the joint capsules.
iii. Systemic lupus erythematosus – autoantibodies attack many
organs
iv. Grave's disease – autoantibodies attack thyroid tissue causing an
excess production of thyroxine.
 v. Type I diabetes mellitus – also known as insulin-dependent
diabetes mellitus (or IDDM), autoantibodies attack the pancreatic
cells that produce insulin.
vi. Glomerulonephritis – autoantibodies attack the kidneys leading to
renal dysfunction.
vii. Myasthenia gravis – attack ACh receptor at neuromuscular
junctions leading to debilitating muscle weakness
viii. Also, see Table 21.7

21.7 Transplantation and Cancer Immunology

1. The Rh Factor
a. RBCs are typed according to surface antigens: A, B, AB, and O
b. Rh factor is another surface protein; presence or absence is indicated by the
positive (+) or negative (-) in a person’s blood type
c. Erythroblastosis fetalis – hemolytic disease of the newborn; Rh-negative
birth parent has multiple Rh-positive children; first pregnancy leads to
development of anti-Rh antibodies which can attack the blood cells of a
second fetus
2. Tissue Transplantation
a. MHC molecules lead to tissue transplant rejection when donor organ
expresses different MHC profile than recipient
b. MHC polygeny = refers to multiple MHC proteins on cells
c. MHC polymorphism = refers to multiple alleles for each MHC locus
d. Tissue typing – matching MHC molecules on donated tissue with recipient
e. Immunosuppressant drugs can help prevent rejection, but matching MHCs is
still key; related donors are more likely to share MHCs
f. Graft-versus-host disease – can occur in bone marrow transplants because
recipient’s immune cells have been destroyed prior to transplantation, and
donor cells may attack recipient tissues
3. Immune Responses Against Cancer
a. Some cancers, like Kaposi’s sarcoma, are well-controlled by a healthy
immune system; caused by herpesvirus, it rarely occurs in
immunocompetent individuals
b. Liver cancer, caused by Hepatitis B virus and cervical cancer, caused by HPV,
can be vaccinated against
c. Immune response to cancer includes three phases: elimination, equilibrium,
and escape