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Title: Chapter 43: Internal Defense


1
Chapter 43 Internal Defense
2
Immune Response fight antigens
  • Nonspecific (innate) general
  • Specific (adaptive or acquired) tailor made
  • Antibodies

3
Fig. 43-2
Pathogens (microorganisms and viruses)
Barrier defenses Skin Mucous membranes Secretions
INNATE IMMUNITY
Recognition of traits shared by broad ranges of
pathogens, using a small set of receptors

Internal defenses Phagocytic cells Antimicrobial
proteins Inflammatory response Natural killer
cells

Rapid response
Humoral response Antibodies defend
against infection in body fluids.
ACQUIRED IMMUNITY

Recognition of traits specific to
particular pathogens, using a vast array of
receptors
Cell-mediated response Cytotoxic lymphocytes
defend against infection in body cells.

Slower response
4
Nonspecific defense
  • Skin
  • Mucus membranes
  • Acid secretions / enzymes of stomach
  • Hairs in nose
  • Phagocytes

5
Cytokines signaling molecules
  • Interferons
  • Interleukins
  • Tumor necrosis factors

6
  • Interferons
  • Secreted by cells infected with viruses,
    parasites
  • Produced by macrophages
  • Type I interferons
  • Inhibit viral replication
  • Viruses exposed to Type I interferon cant infect
    other cells as well
  • Activate natural killer cells
  • Type II interferons
  • Specific immune system
  • Enhance activities of other immune cells
  • Stimulate macrophages to destroy tumor cells and
    virus-infected cells

7
  • Interleukins
  • Secreted by macrophages and lymphocytes
  • Regulate actions between lymphocytes and other
    body cells
  • Interleukin-1 can reset bodys thermostat in
    hypothalamus resulting in fever

8
  • Tumor necrosis factors (TNFs)
  • Secreted by macrophages and lymphocytes
  • Stimulate immune cells for inflammation
  • Kill tumor cells

9
Complement system
  • Complements actions of other defenses
  • 20 proteins in body fluids
  • Inactive until body exposed to antigen
  • Sometimes activated directly OR by binding of
    antigen to antibody
  • Nonspecific
  • 4 actions
  • Lyse pathogen cell wall
  • Coat pathogen (phagocytes can work more easily)
  • Attract WBCs to infected site
  • Increase inflammation by stimulating release of
    histamine

10
Phagocytosis
  • Nonspecific
  • Phagocytes
  • neutrophils (20 bacteria)
  • Macrophages (100 bacteria)
  • Endocytosis

11
Fig. 43-3
Microbes
PHAGOCYTIC CELL
Vacuole
Lysosome containing enzymes
12
Natural Killer (NK) Cells
  • Large, granular lymphocytes
  • Bone marrow
  • Nonspecific and specific
  • Release cytokines and enzymes to destroy target
    cells

13
Inflammation
  • Heat, redness, edema, pain
  • Regulated by plasma proteins, cytokines, platelet
    substances, basophils, mast cells
  • Blood vessels dilate
  • Increase capillary permeability
  • Increase blood flow lots neutrophils,
    phagocytes, platelets, basophils, mast cells to
    infected area
  • Mast cells release histamine, serotonin
  • Increase blood flow ? skin warm, appears red
  • Phagocytes go out of capillaries to infected
    tissue (phagocytosis)

14
  • Edema fluid and antibodies leave circulation to
    enter tissues
  • Swelling increased volume of fluid in area
  • Pain from edema and action of enzymes in plasma

15
Fig. 43-8-3
Pathogen
Splinter
Chemical signals
Macrophage
Fluid
Mast cell
Capillary
Phagocytosis
Red blood cells
Phagocytic cell
16
Fever
  • Bodys thermostat in hypothalamus reset
  • Higher temp. interferes with growth and
    replication of some pathogens
  • Lysosomes break down, destroying cells infected
    by viruses
  • Increased temp. promotes T cell activity and
    production of antibodies
  • Increased phagocytosis

17
Specific immune response
  • 2 types
  • Antibody-mediated immunity
  • Cell-mediated immunity

18
Fig. 43-16
Humoral (antibody-mediated) immune response
Cell-mediated immune response
Key
Antigen (1st exposure)
Stimulates Gives rise to

Engulfed by
Antigen- presenting cell



B cell
Helper T cell
Cytotoxic T cell


Memory Helper T cells



Antigen (2nd exposure)
Memory Cytotoxic T cells
Active Cytotoxic T cells

Plasma cells
Memory B cells
Secreted antibodies
Defend against extracellular pathogens by binding
to antigens, thereby neutralizing pathogens or
making them better targets for phagocytes and
complement proteins.
Defend against intracellular pathogens and cancer
by binding to and lysing the infected cells or
cancer cells.
19
Lymphocytes
  • 3 types
  • T cells
  • B Cells
  • NK cells

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Natural Killer cells
  • Kill virally infected and tumor cells

22
B cells
  • Antibody-mediated immunity
  • Mature into plasma cells (produce specific
    antibodies)
  • Encode a receptor that binds to a specific
    antigen
  • B cell receptors bind to antigen ? B cell
    activated
  • Divides rapidly ? differentiate into plasma cells
    which produce antibody
  • Antibody binds to antigen that originally
    activated B cells

23
  • Some become memory B cells
  • Continue to make small amounts of antibody after
    infection has been overcome

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Fig. 43-19-3
Bacterium
Antigen-presenting cell
Peptide antigen
B cell
Class II MHC molecule
Secreted antibody molecules
Clone of plasma cells

TCR
CD4
Cytokines
Activated helper T cell
Helper T cell
Clone of memory B cells
26
Fig. 43-14
Antigen molecules

B cells that differ in antigen specificity
Antigen receptor
Antibody molecules
Clone of memory cells
Clone of plasma cells
27
Role of B Cells Animation
28
T cells
  • Cell-mediated immunity
  • T thymus-derived
  • Thymus make T cells immunocompetent
  • In thymus cells divided many times, develop
    specific surface proteins with distinctive
    receptor sites
  • Attack body cells infected by invading pathogens,
    foreign cells, cancer cells

29
  • T cell antigen receptor (TCR)
  • Distinguishes T cells
  • Allows T cells to recognize specific antigens
  • 2 main types
  • CD8 T cells (surface marker CD8)
  • Cytotoxic T cells (killer T cells)
  • Recognize/destroy foreign antigens
  • Targets? virus-infected cells, cancer cells,
    foreign tissue grafts
  • Kill by releasing variety of cytokines and
    enzymes to lyse cells

30
Fig. 43-18-3
Released cytotoxic T cell
Cytotoxic T cell
Perforin
Granzymes
CD8
TCR
Dying target cell
Class I MHC molecule
Pore
Target cell
Peptide antigen
31
  • CD4 T cells (surface marker CD4)
  • Helper T cells
  • Secrete substances that activate or enhance
    immune responses
  • 2 subsets
  • T helper 1 cell-mediated
  • T helper 2 antibody- mediated stimulate B
    cells divided and produce antibodies

32
Fig. 43-17
Antigen- presenting cell
Peptide antigen
Bacterium
Class II MHC molecule
CD4
TCR (T cell receptor)
Helper T cell

Cytokines
Humoral immunity (secretion of antibodies
by plasma cells)

Cell-mediated immunity (attack on infected cells)


B cell
Cytotoxic T cell
33
Fig. 43-12
Antigen- presenting cell
Microbe
Infected cell
Antigen associates with MHC molecule
1
Antigen fragment
Antigen fragment
1
1
Class I MHC molecule
Class II MHC molecule
2
2
T cell receptor
T cell receptor
2
T cell recognizes combination
(a)
Cytotoxic T cell
(b)
Helper T cell
34
Major Histocompatibility complex
  • MHC antigens cell surface proteins
  • Help vertebrates distinguish self vs. nonself
  • Coded for by set of closely linked genes Major
    histocompatibility complex (MHC)
  • Humans MHC HLA (human leukocyte antigen)
  • Polymorphic
  • Many combination ? not likely for people to have
    same combo (except identical twins)

35
Antibody-mediated Immunity
  • (humoral immunity)
  • B cells responsible
  • Produce surface receptors
  • Bind to particular antigen
  • B cell activates

36
  • Foreign antigen displayed on immune cell surface
  • Contacts helper T cell (has complementary
    receptors)
  • Macrophage secretes IL-1 activated helper T
    cells
  • (T cells do not recognize an antigen presented
    alone)
  • Antibody receptor of B cell binds with
    complementary antigen

37
  • Inside B cell antigen degraded ? peptide
    fragments
  • B cells display fragments on surface
  • Activated helper T binds with B cells
  • Activated helper T releases interleukins which,
    with antigen, activate B cell
  • B cell increases in size ? mitosis
  • Each new cells makes antibodies specific to
    antigen from original B cell

38
  • Some cells of B cell clone ? plasma cells
  • Secrete antibody specific to antigen
  • Plasma cells do not leave lymph nodes
  • Antibodies can pass out of lymph tissue to
    infected area

39
  • Some B cells ? memory B cells
  • Live and make antibody after infection gone
  • Same pathogen enters later ? circulating antibody
    targets it for destruction
  • Same time ? memory cells divided ? plasma cells

40
Helper T Cell Activation
41
Fig. 43-9
Antigen- binding site
Antigen- binding site
Antigen- binding site



Disulfide bridge
V
V
V
V
Variable regions
V
V
C
C
Constant regions
C
C
C
C
Light chain
Transmembrane region


Plasma membrane
? chain
? chain
Heavy chains
Disulfide bridge
T cell
Cytoplasm of T cell
Cytoplasm of B cell
B cell
(b) T cell receptor
(a) B cell receptor
42
Fig. 43-9a
Antigen- binding site
Antigen- binding site


Disulfide bridge
V
V
V
V
Variable regions
C
C
Constant regions
C
C
Light chain
Transmembrane region

Plasma membrane
Heavy chains
Cytoplasm of B cell
B cell
(a) B cell receptor
43
Fig. 43-9b
Antigen- binding site

Variable regions
V
V
Constant regions
C
C
Transmembrane region

Plasma membrane
? chain
? chain
Disulfide bridge
T cell
Cytoplasm of T cell
(b) T cell receptor
44
Antibodies
  • (immunoglobulin, Ig)
  • 2 main functions
  • Combines with antigen
  • Activate processes to destroy antigen
  • Labels antigen for destruction
  • Doesnt destroy antigen directly

45
Structure of Antibody
  • 4 polypeptide chains
  • 2 identical long chains ? heavy chains
  • 2 identical short chains ? light chains
  • Can bind with different affinities
  • During immune response, higher affinity
    antibodies are made

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Antigenic determinant
  • Give antigen specific shape to be recognized by
    antibody
  • Usually antigen has many different antigenic
    determinants
  • Many antibodies can bind to antigen

48
Fig. 43-10
Antigen- binding sites
Epitopes (antigenic determinants)
Antigen-binding sites


Antigen
Antibody A
Antibody C
V
V
V
V
C
C
C
C
Antibody B
49
5 Classes of Antibodies
  • Unique AA sequences in heavy chain
  • 1. IgG human 75
  • Gamma globulin fraction of plasma
  • Interact with macrophages, activate complement
    system
  • 2. IgM
  • Interact with macrophages, activate complement
    system
  • Defend against pathogens in blood

50
  • 3. IgA
  • Mucus, tears, saliva, milk
  • Body openings
  • 4. IgD
  • Low concentration in plasma
  • Helps activate B cells after antigen binding
  • 5. IgE
  • Low concentration in plasma
  • Can bind to mast cells, cells with histamine
    (allergy)
  • Parasitic worms

51
Fig. 43-20a
Class of Immuno- globulin (Antibody)
Distribution
Function
First Ig class produced after initial exposure
to antigen then its concentration in the blood
declines
Promotes neutraliza- tion and cross- linking of
antigens very effective in complement
system activation
IgM (pentamer)
J chain
52
Fig. 43-20b
Class of Immuno- globulin (Antibody)
Distribution
Function
IgG (monomer)
Most abundant Ig class in blood also present
in tissue fluids
Promotes opsoniza- tion, neutralization, and
cross-linking of antigens less effec- tive in
activation of complement system than IgM
Only Ig class that crosses placenta, thus
conferring passive immunity on fetus
53
Fig. 43-20c
Class of Immuno- globulin (Antibody)
Distribution
Function
IgA (dimer)
Present in secretions such as tears,
saliva, mucus, and breast milk
Provides localized defense of mucous membranes
by cross-linking and neutralization of antigens
J chain
Presence in breast milk confers passive
immunity on nursing infant
Secretory component
54
Fig. 43-20d
Class of Immuno- globulin (Antibody)
Distribution
Function
IgE (monomer)
Present in blood at low concen- trations
Triggers release from mast cells and basophils of
hista- mine and other chemicals that
cause allergic reactions
55
Fig. 43-20e
Class of Immuno- globulin (Antibody)
Distribution
Function
IgD (monomer)
Present primarily on surface of B cells that
have not been exposed to antigens
Acts as antigen receptor in the antigen-stimulated
proliferation and differentiation of B cells
(clonal selection)
Trans- membrane region
56
Antibody Antigen activates other defense
mechanisms
  • 1. inactivate pathogen or its toxin
  • Ex virus may not be able to attach to host
  • 2. stimulates phagocytic cells to ingest the
    pathogen
  • 3. complement proteins destroy pathogens
  • IgG and IgM Fc fragments bind to phagocytes for
    destruction

57
Monoclonal Antibodies
  • identical antibodies produced by cells cloned
    from a single cell
  • Steps
  • Inject specific antigen into mice
  • Mice make antibodies
  • Collect mice B cells
  • Mix B cells (can only live in culture a few
    generations) with lymphoma cells (can live in
    tissue culture indefinitely)

58
  • Cells induced to fuse ? hybrid cells hybridomas
  • Have properties of 2 parent cells
  • B cells secrete antibodies
  • Cancer cells cultured indefinitely
  • Select hybrid cells making specific antibody
  • Clone them
  • Cells of clone make large amounts of specific
    antibody

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Antibodies Animation
61
Cell Mediated Immunity
  • T cells and APCs responsible
  • T cells destroy virus-infected cells, altered
    cells (cancer cells), foreign grafts
  • Steps
  • Virus invades body cells
  • Viral proteins displayed on cell surface of APC
  • T cells with specific receptor to that antigen
    become activated
  • T cell grows in size ? clone of helper T cells,
    cytotoxic T cells and memory T cells

62
  • Cytotoxic T cells leave lymph nodes ? infected
    area
  • Combine with antigen on target cell
  • Releases cytotoxic proteins to destroy cell
  • Disengages from target and seeks new one

63
Cytotoxic T Cells animation
64
Long-term Immunity and Immunological Memory
  • Memory B and memory T cell responsible
  • Primary Response vs. Secondary Response

65
Primary Response
  • 1st exposure to antigen
  • 3-14 days for specific antibodies
  • Injection of antigen
  • Brief latent period ? antigen is recognized and
    appropriated lymphocytes form clones
  • Logarithmic phase ? antibody concentration rises
    rapidly for several days (mostly IgM)
  • Decline phase ? antibody concentration decreases
    to very low level

66
Secondary Response
  • 2nd injection of same antigen
  • More rapid
  • Shorter latent period ? memory B and T cells
    already bear antibodies to that antigen
  • Less antigen needed for response
  • More antibodies made with higher affinity (mostly
    IgG)
  • Why we dont usually suffer same disease many
    times
  • No symptoms
  • Booster shots elicit secondary response to
    reinforce immunological memory

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Active immunity
  • Developed after exposure to antigens
  • Naturally or artificially induced
  • Immunization - Exposed to vaccine
  • Virus attenuated
  • Sabin polio, measles
  • Killed pathogens ( still have antigens)
  • Whooping cough, Typhoid fever
  • Toxins from pathogens (altered so no destruction,
    same antigens)
  • Tetanus, botulism

69
Passive Immunity
  • Individual is given antibodies actively produced
    by another organism
  • borrowed immunity effects dont last
  • Used to boost bodys defense temporarily
  • Natural passive immunity
  • Mom ? baby
  • Through placenta
  • Until babys own immune system matures
  • IgA in breast milk

70
Cancer
  • Precancer cells different surface proteins
    (antigens)
  • Dendritic cells recognize, present cancer antigen
    to T cells
  • T cell activates ? clone cytotoxic T cells, make
    interleukins to attract macrophages and NK cells
  • Cytotoxic T cells make interferons for antitumor
    effect
  • Macrophages make TNF to inhibit tumor growth

71
Graft Rejection and Transplants
  • MHC antigens same only for identical twins
  • Hard to find matches because so many
    possibilities for MHC antigens
  • Graft rejection immune response against a
    foreign graft/transplant
  • T cells attack transplanted tissue, destroy in a
    week
  • To prevent rejection
  • Drugs suppress immune system

72
  • Xenotransplantation process to transplant
    animal parts to humans
  • Genetic engineered pigs
  • Artificial organs

73
Allergic reactions
  • Hypersensitivity results in the manufacture of
    antibodies against mild antigens, called
    allergens, that normally do not stimulate an
    immune response
  • Ex dust mites, pollen

74
Common allergic reactionEx hayfever to ragweed
pollen
  • Sensitization
  • Activation of mast cells
  • Allergic response prolonged (maybe)

75
Sensitization
  • Macrophages degrade allergen, present fragments
    of it to T cells
  • Activated T cells stimulate B cells into plasma
    cells and produce IgE
  • IgE antibodies attach to receptors on mast cells
    (at C region V region is left open to attach to
    allergen)

76
Activation of Mast cells
  • Allergens attach to IgE on mast cells stimulating
    mast cells to release histamine and serotonin
    that cause inflammation
  • Blood vessels dilate
  • Capillaries more permeable ? edema, red
  • Nasal passages swollen, irritated
  • Noses run, sneeze, eyes water

77
Allergic response is prolonged (maybe)
  • Chemical from mast cells lure certain WBCs to
    inflamed area
  • WBCs release compounds that damage tissue and
    prolong reaction

78
Fig. 43-23
IgE
Histamine
Allergen
Granule
Mast cell
79
Hives
  • Allergen/IgE reaction happens in skin
  • Histamine released by mast cells causes swollen
    red welts (hives)

80
Systemic anaphylaxis
  • Dangerous allergic reaction that can occur when a
    person develops an allergy to a specific drug,
    venom or food
  • In minutes ? widespread reaction
  • Mast cells give off much histamine ? vasodilation
    and permeability
  • So much plasma may be last from blood that
    circulatory shock and death can occur in minutes

81
Antihistamines
  • Drugs that block the effects of histamines
  • Compete for same receptors on target cells as
    histamine
  • Not totally effective because mast cells release
    substances other than histamine for reaction

82
Autoimmunity
  • T cells react immunologically against self
  • Ex
  • Rheumatoid arthritis
  • Multiple sclerosis
  • Systemic lupus erythematosus
  • Insulin-dependent diabetes
  • Psoriasis
  • Scleroderma
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