Chapter 43 Internal Defense

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Transcript Chapter 43 Internal Defense

Biology, Seventh Edition
Solomon • Berg • Martin
Chapter 43
Internal Defense
Copyright © 2005 Brooks/Cole — Thomson Learning
Biology, Seventh Edition
CHAPTER 43 Internal Defense
• Immunology
• Study of internal defensive
responses
• Immune response
• Recognizing foreign or
dangerous macromolecules
• Responding to eliminate them
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CHAPTER 43 Internal Defense
Human immune response
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CHAPTER 43 Internal Defense
• Nonspecific immune responses
• Provide general and immediate
protection
–Pathogens
–Some toxins and drugs
–Cancer cells
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• Specific immune responses
• Highly specific
• Include immunological memory
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• Antigen
• Molecule specifically recognized
as foreign or dangerous by cells
of the immune system
• Antibodies
• Highly specific proteins that
recognize and bind to specific
antigens
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CHAPTER 43 Internal Defense
• Invertebrate immune responses
• Always nonspecific
• Physical barriers
–Cuticle
–Skin
–Mucous membranes
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CHAPTER 43 Internal Defense
• Phagocytosis
• Antimicrobial peptides
–Soluble molecules that destroy
pathogens
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CHAPTER 43 Internal Defense
Phagocytosis
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CHAPTER 43 Internal Defense
• Vertebrate nonspecific immune
responses
• First-line defenses
–Physical barriers
–Skin
–Mucous linings of the respiratory
and digestive tracts
• Other nonspecific defenses
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• Soluble molecules important in
immune responses
• Antimicrobial peptides
• Regulatory peptides
• Proteins that destroy pathogens
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CHAPTER 43 Internal Defense
• Cytokines
• Signaling proteins that regulate
interactions between cells
• Interferons
–Inhibit viral replication and activate
natural killer cells
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• Interleukins
–Help regulate interactions between
lymphocytes and other cells of the
body
–Some have widespread effects
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• Chemokines
–Attract, activate, and direct the
movement of certain cells of the
immune system
• Tumor necrosis factors (TNFs)
–Kill tumor cells and stimulate
immune cells to initiate an
inflammatory response
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• Complement proteins
• Enhance the inflammatory
response
–Lyse the cell wall of pathogens
–Coat pathogens, enhancing
phagocytosis
–Attract white blood cells to the site
of infection
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• Phagocytes destroy bacteria
• Neutrophils
• Macrophages
• Natural killer cells (NK cells)
• Destroy cells infected with
viruses
• Destroy foreign or altered cells
such as tumor cells
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CHAPTER 43 Internal Defense
• Inflammatory response
• Triggered when pathogens
invade tissues
• Vasodilation
–Increased blood vessel diameter
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• Increased capillary permeability
–Allows fluid and antibodies to leave
the circulation and enter the tissues
• Increased phagocytosis
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• In response to tissue injury,
several types of molecules in
the plasma that mediate
inflammation are activated
• Mast cells release histamine
and other compounds that
cause vasodilation and
increased capillary permeability
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CHAPTER 43 Internal Defense
• Cell-mediated immunity
• Specific T cells are activated
• Proteins released that destroy
cells infected with viruses or
other intracellular pathogens
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• Antibody-mediated immunity
• Specific B cells are activated
• Multiply and differentiate into
plasma cells, which produce
antibodies
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• Immune system cells
• Lymphocytes
–Develop from stem cells in the bone
marrow
–T cells
–B cells
• Antigen-presenting cells (APCs)
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Lymphocytes and antigen-presenting cells
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• T cells
• Responsible for cell-mediated
immunity
• T cytotoxic cells (TC cells)
• T helper cells (TH)
• Memory T cells
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• Distinguished by T-cell receptors
(TCRs)
• Thymus gland confers
immunocompetence on T cells by
making them capable of
distinguishing between self and
non-self
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• B cells
• Responsible for antibodymediated immunity
• Differentiate into plasma cells
–Produce antibodies
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• Some activated B cells become
memory B cells
–Continue to produce antibodies
after an infection has been
overcome
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• Antigen-presenting cells (APCs)
• Display foreign antigens as well
as their own surface proteins
• Macrophages
• B cells
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• Dendritic cells
–Located in tissues that interact with
the environment
–Specialized to process, transport,
and present antigens
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• Major histocompatibility
complex (MHC)
• Immune responses depend on a
group of genes that encode MHC
proteins
• Class I MHC genes
–Encode self antigens, glycoproteins
expressed on the surface of most
nucleated cells
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• Class II MHC genes
–Encode glycoproteins expressed on
APCs of the immune system
• Class III MHC genes
–Encode components of the
complement system and TNFs
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• Cell-mediated immunity process
• Specific T cells are activated by a
foreign antigen–MHC complex on
the surface of an infected cell
• A co-stimulatory signal and
interleukins are also required
• Activated TC cells multiply, giving
rise to a clone
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• Clone cells migrate to the site of
infection
• Pathogen-infected cells
destroyed
• Activated TH cells give rise to a
clone of TH cells
• Clone cells secrete cytokines
• B cells and macrophages
activated
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• Antibody-mediated immunity
process
• B cells are activated when they
combine with antigen
• Activation requirements
–APC (dendritic cell or macrophage)
with a foreign antigen–MHC
complex displayed on its surface
–TH cell that secretes interleukins
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• Activated B cells multiply, giving
rise to clones of cells
• Cloned cells differentiate, forming
plasma cells
• Plasma cells produce specific
antibodies, immunoglobulins (Ig),
in response to the specific
antigens that activated them
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• An antibody combines with a
specific antigen to form an
antigenantibody complex
–May inactivate the pathogen
–Stimulate phagocytosis
–Activate the complement system
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• Antibody structure
• Y-shaped
• Two arms combine with antigen
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Antigenantibody
complex
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• Antibody molecule
• Four polypeptide chains
–Two identical heavy chains
–Two shorter light chains
• Chain regions
–Constant (C) region and
–Variable (V) region
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• Recombination of DNA
segments
• Main factor responsible for
antibody diversity
• Occurs during the differentiation
of B cells
• Millions of different types of B
(and T) cells are produced
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• Immunological memory
• Memory B and memory T cells
remain in the body after an
infection
• Responsible for long-term
immunity
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Immunological memory
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• Primary immune response
• Stimulated by the first exposure
to an antigen
• Secondary immune response
• Stimulated by a second exposure
to the same antigen
• More rapid and more intense
than the primary response
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• Active immunity
• Develops as a result of exposure
to antigens
• May occur naturally after
recovery from a disease
• May be artificially induced by
immunization with a vaccine
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• Passive immunity
• Temporary condition
• Develops when an individual
receives antibodies produced by
another person or animal
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CHAPTER 43 Internal Defense
• Response to cancer cells
• NK cells, macrophages, and
T cells recognize antigens on
cancer cells and launch an
immune response against them
• Cancer cells evade the immune
system by blocking TC directly or
by decreasing their class I MHC
molecules
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CHAPTER 43 Internal Defense
Cancer cell destruction
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• Human immunodeficiency virus
(HIV)
• Retrovirus
• Causes acquired
immunodeficiency syndrome
(AIDS)
• Destroys T helper cells
• Severely impairs immunity
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HIV-infected T cell
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• Graft rejection
• Transplanted tissues have MHC
antigens
• Immune response stimulated
• T cells destroy the transplant
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CHAPTER 43 Internal Defense
• Hypersensitivity reactions
• Rh incompatibility
• Allergic reactions
• Autoimmune diseases
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CHAPTER 43 Internal Defense
• Rh incompatibility
• Rh-negative woman gives birth to
an Rh-positive baby
• Anti-D antibodies develop
• Rh incompatibility occurs in future
pregnancies
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CHAPTER 43 Internal Defense
Rh incompatibility
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CHAPTER 43 Internal Defense
• Allergic reaction
• Allergen stimulates the
production of IgE
• IgE combines with receptors on
mast cells
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• Mast cells release histamine and
other molecules
–Causes inflammation, other allergy
symptoms
• Systemic anaphylaxis
–Rapid, widespread allergic reaction
–Can lead to death
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CHAPTER 43 Internal Defense
Allergic reaction
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