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Transcript
Anatomy & Physiology
Chapter 24: Immune System
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Introduction

The immune system protects against
assaults on the body


External assaults include
microorganisms—protozoans,
bacteria, and viruses
Internal assaults—abnormal cells
reproduce and form tumors that may
become cancerous and spread
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Organization of the Immune System


Immune system continually patrols and protects
the body
Identification of cells and other particles




Markers, or antigens, are unique molecules recognized by the
immune system
Self markers—molecules on the surface of our cells that are
unique to an individual, thus identifying the cell as “self” to the
immune system
Nonself markers—molecules on the surface of foreign or
abnormal cells or particles that identify the particle as
“nonself” to the immune system
Self-tolerance—the ability of our immune system to attack
abnormal or foreign cells but spare our own normal cells
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Organization of the Immune System

Two major categories of immune mechanisms—
innate immunity and adaptive immunity (Figure
24-1; Table 24-1)



Innate immunity provides a general, nonspecific defense
against anything that is not “self”
Adaptive immunity acts as a specific defense against
specific threatening agents
Primary cells of innate immunity—epithelial barrier cells,
phagocytes (neutrophils, macrophages, DCs), and natural
killer cells; chemicals used in innate immunity—
complement and interferon
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Organization of the Immune System

Two major categories of immune
mechanisms (cont)



Primary cells of adaptive immunity—
lymphocytes called T cells and B cells
Cytokines—chemicals released from cells
to promote or trigger innate and adaptive
immune responses (e.g., interleukin,
interferon, leukotriene)
Other chemicals (e.g., complement, other
enzymes, histamine) also play regulatory
roles in immunity
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Innate Immunity (Table 24-2)


Species resistance—genetic characteristics of
an organism or species defend against
pathogens
Mechanical and chemical barriers—first line of
defense (Figure 24-2)


Internal environment of the body is protected by a
barrier formed by the skin and the mucous
membranes
Skin and mucous membranes provide additional
immune mechanisms—sebum, mucus, enzymes,
and hydrochloric acid in the stomach
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Innate Immunity

Inflammation and fever—second line of defense
(Figure 24-3)

Inflammatory response—tissue damage elicits responses to
counteract injury and promote normalcy




Inflammation mediators include histamine, kinins,
prostaglandins, and related compounds (Figure 24-4)
Chemotactic factors—substances that attract white blood
cells to area of injury in a process called chemotaxis
(Figure 24-6)
Characteristic signs of inflammation—heat, redness, pain,
and swelling
Systemic inflammation—occurs from a bodywide
inflammatory response
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Innate Immunity

Inflammation and fever (cont)

Fever—abnormally high body
temperature triggered by
inflammation mediators
 Triggered in SIRS (systemic
inflammatory response
syndrome) and other events
such as viral infections, tumors,
allergies
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Innate Immunity

Fever (cont)
 Pyrogens released from damaged tissues
(endogenous) or introduced into the body
(exogenous)
 Promote prostaglandin (PG) production
 PGs reset the hypothalamic
“thermostat” to a higher temperature
 Aspirin and other COX inhibitors
interfere with PG production
 Fever is thought to increase immune
function and inhibit pathogens
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Innate Immunity

Phagocytosis—ingestion and destruction of
microorganisms or other small particles by
phagocytes (Figure 24-7)


Phagocytes—many types capable of phagocytosis
(Table 24-3)
Antigen-presenting cells (APCs)—phagocytes that
ingest foreign particles, isolate protein segments
(peptides), and display them as antigens on their
surface to trigger an immune response when
recognized by a specific (adaptive) immune cell

Neutrophil—most numerous phagocyte; usually
first to arrive at site of injury; migrates out of
bloodstream during diapedesis; form pus
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Innate Immunity

Antigen-presenting cells (cont)




Diapedesis—process by which immune cells
squeeze through the wall of a blood vessel to
get to the site of injury or infection (Figure 24-5)
Macrophage—large phagocytic monocyte cells
that grow to several times original size after
migrating out of bloodstream; important APCs
Dendritic cell (DC)—type of APC with long
branches or extensions (Figure 24-8)
Phagocytes often identified by location—
histiocytes in connective tissue, microglia in
nervous system, and Kupffer cells in liver
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Innate Immunity

Natural killer (NK) cells—lymphocytes
that kill tumor cells and cells infected by
viruses (Figure 24-9)


Method of recognizing abnormal or
nonself cells—target cell is killed if killerinhibiting receptor on NK cell does not
bind to a proper MHC surface protein
Method of killing cells—lysing cells by
damaging plasma membranes
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Innate Immunity


Interferon (IFN)—protein synthesized and
released into circulation by certain cells if
invaded by viruses to signal other nearby cells
to enter a protective antiviral state
Complement—group of enzymes that produce a
cascade of reactions resulting in a variety of
immune responses (Figure 24-10)



Lyse cells when activated by either adaptive or
innate mechanisms
Opsonization—process that marks cells for
destruction by phagocytes
Variety of other immune responses (Figure 24-10)
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Innate Immunity

Toll-like receptors (TLRs)—patternrecognition receptors in the
membranes of host cells; when
triggered, TLRs stimulate many
different kinds of innate immune
responses
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Overview of Adaptive Immunity

Adaptive immunity


Part of the third line of defense
consisting of lymphocytes
Two different classes of a white blood
cell (lymphocyte) involved (Figure 2411)
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Overview of Adaptive Immunity

Classes of lymphocytes (Figure 2412)—B lymphocytes (B cells) and T
lymphocytes (T cells)


B-cell mechanisms—antibodymediated immunity (humoral
immunity); produce antibodies that
attack pathogens (Figure 24-13)
T cell mechanisms—attack pathogens
more directly—classified as cellmediated immunity (cellular immunity)
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Overview of Adaptive Immunity

Classes of lymphocytes (cont)


Lymphocytes have protein markers on their
surfaces
 Surface markers named using the CD
(cluster of differentiation) system
 Examples include CD4 and CD8 cells,
clinically important in diagnosing AIDS
Activation of lymphocytes requires two
stimuli: a specific antigen and activating
chemicals (Figure 24-14)
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Overview of Adaptive Immunity

Classes of lymphocytes (cont)


Lymphocytes are densest where they
develop—in bone marrow, thymus
gland, lymph nodes, and spleen
(Figure 24-15)
Lymphocytes flow through the
bloodstream, become distributed in
tissues, and return to the bloodstream
in a continuous recirculation
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B Cells and
Antibody-Mediated Immunity

Development and activation of B cells

Development occurs in two stages (Figure 24-16)
• Pre–B cells develop in red bone marrow (prenatal, in the
yolk sac and fetal liver)
• Second stage occurs in lymph nodes and spleen—
activation of a naïve B cell after it binds to a specific
antigenic. B cells divide repeatedly—serve as ancestors to
antibody-secreting plasma cells


Some of the clone cells differentiate to form B cells or plasma
cells
Others remain in lymphatic tissue and become memory B cells
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B Cells and
Antibody-Mediated Immunity

Antibodies—proteins
(immunoglobulins) secreted by
activated B cell (Figure 24-16)

Structure of antibody molecules
• An antibody molecule consists of two
heavy and two light polypeptide chains
• Each molecule has two antigen-binding
sites and two complement-binding sites
(Figure 24-17)
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B Cells and
Antibody-Mediated Immunity

Antibodies (cont)

Diversity of antibodies
• Babies are born with different clones of
B cells in bone marrow, lymph nodes,
and spleen
• Cells of the clone synthesize a specific
antibody with a sequence of amino
acids in its variable region that differs
from the sequence synthesized by other
clones
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B Cells and
Antibody-Mediated Immunity

Antibodies (cont)

Classes of antibodies (Figure 24-18)—
immunoglobulins M, G, A, E, and D
• IgM—antibody that naïve B cells synthesize
and insert into their own plasma membranes;
the predominant class produced after initial
contact with an antigen
• IgG—makes up 75% of antibodies in the blood;
predominant antibody of the secondary
antibody response
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B Cells and
Antibody-Mediated Immunity

Classes of antibodies (cont)
• IgA—major class of antibody in the mucous
membranes, in saliva and tears (also found
in plasma)
• IgE—small amount; produces harmful
effects such as allergies
• IgD—small amount in blood; precise
function unknown
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B Cells and
Antibody-Mediated Immunity

Antibodies (cont)

Functions of antibodies (Figure 24-19)
• Antigen-antibody reactions
 Transforms toxic antigens into harmless
substances
 Agglutinates antigens to make disposal by
phagocytes more rapid
 Alters the shape of antigen molecule to
expose complement-binding sites (Figure
24-20)
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B Cells and
Antibody-Mediated Immunity

Functions of antibodies (cont)
• Complement—a component of blood
plasma consisting of several protein
compounds (inactive enzymes)
 Antibodies can activate complement
after binding to an antigen by exposing
complement-binding sites that trigger a
cascade of linked chemical reactions to
produce a variety of immune effects
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B Cells and
Antibody-Mediated Immunity

Antibodies can activate complement after
binding (cont)


Membrane attack complex (MAC)—
complement cascade can form doughnutshaped structures that produce a hole in a
foreign cell’s membrane, causing cytolysis
(cell rupture) (Figures 24-21 and 24-22)
Complement can also cause vasodilation,
enhances phagocytosis, and has other effects
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B Cells and
Antibody-Mediated Immunity
• Complement (cont)

Complement activity can also be initiated by
innate immune mechanisms
 Complement protein 3 (C3)—activated
without antigen stimulation—produces
full complement effect by binding to
bacteria or viruses in presence of
properdin
 Complement activation by innate
immunity is called the alternate pathway
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B Cells and
Antibody-Mediated Immunity

Functions of antibodies (cont)
• Primary and secondary responses (Figure 24-23)
 Primary response—initial encounter with a
specific antigen triggers the formation and
release of specific antibodies that reaches its
peak in a few days
 Secondary response—a later encounter with
the same antigen triggers a much quicker
response; B memory cells rapidly divide,
producing more plasma cells and thus more
antibodies
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B Cells and
Antibody-Mediated Immunity

Clonal selection theory (Figure 24-24)

Two basic tenets
Body contains many diverse clones of cells, each
committed by its genes to synthesize a different antibody
 When an antigen enters the body, it selects the clone
whose cells are synthesizing its antibody and stimulates
them to proliferate and create more antibody
The clones selected by antigens consist of lymphocytes and
are selected by the shape of antigen receptors on the
lymphocyte’s plasma membrane


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T Cells and Cell-Mediated Immunity

Development of T cells



T Cells are lymphocytes that go through
the thymus gland before migrating to the
lymph nodes and spleen
Pre–T cells develop into thymocytes
while in the thymus
Thymocytes stream into the blood and
are carried to the T-dependent zones in
the spleen and the lymph nodes
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T Cells and Cell-Mediated Immunity

Activation of T cells


T cells display antigen receptors on their surface membranes
that are similar to antibodies
A T cell is activated when an antigen (in an infected cell or
presented by an APC) binds to its receptors (at an IS),
causing the T cell to divide repeatedly to form a clone of
identical T cells (Figure 24-25)



Cells of the clone differentiate into effector T cells and
memory T cells
Effector T cells go to the site where the antigen entered,
bind to antigens, and begin their attack
Memory T cells remain in bone marrow until needed later to
produce more effector T cells and memory T cells
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T Cells and Cell-Mediated Immunity

Functions of T cells




Cytotoxic T cells—T cells release lymphotoxin to kill
cells (Figure 24-26)
Helper T cells (TH cells)—regulate the function of B
cells, T cells, phagocytes, and other leukocytes
(Figure 24-27)
Suppressor T cells—regulatory T cells that suppress
lymphocyte function, thus regulating immunity and
promoting self tolerance
T cells function to produce cell-mediated immunity
and help to regulate adaptive immunity in general
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Types of Adaptive Immunity
(Table 24-4)


Innate immunity (inborn or inherited immunity)—
genetic mechanisms put innate immune
mechanisms in place during development in the
womb
Adaptive or acquired immunity; resistance
developed after birth; two types:


Natural immunity results from nondeliberate
exposure to antigens
Artificial immunity results from deliberate
exposure to antigens, called immunization
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Types of Adaptive Immunity

Natural and artificial immunity may be
active or passive


Active immunity—when the immune system
responds to a harmful agent regardless of
whether it was natural or artificial; lasts
longer than passive
Passive immunity—immunity developed in
another individual is transferred to an
individual who was not previously immune;
it is temporary but provides immediate
protection
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Summary of Adaptive Immunity


Adaptive immunity is specific
immunity—targeting specific antigens
Adaptive immunity involves two
classes of lymphocyte: B cells and T
cells (Figure 24-27)


B cells—antibody-mediated (humoral)
immunity
T cells—cell-mediated (cellular)
immunity
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Summary of Adaptive Immunity

Adaptive immunity occurs in a series of stages
(Figure 24-28)

Recognition of antigen

Activation of lymphocytes

Effector phase (immune attack)



Decline of antigen causes lymphocyte death
(homeostatic balance)
Memory cells remain for later response if needed
B cells and T cells work together in a coordinated
system of adaptive immunity (Figure 24-29)
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The Big Picture: Immune System
and The Whole Body


Immune system regulated to some
degree by nervous and endocrine
systems
Agents of the immune system include
blood cells, skin cells, mucosal cells,
brain cells, liver cells, and other types
of cells and their secretions
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