Bio 1b Zoology Hannah Nevins Immunity: the bodys defense system
An immune cell (macrophage) engulfs a yeast cell (pathogen)
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Invaders : pathogens The immune system recognizes foreign
bodies and responds with the production of immune cells and
proteins Two strategies have evolved: the innate and the acquired
immune systems
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Benjamin Cummings Innate Immunity of Invertebrates The digestive
system is protected by low pH and an enzyme that digests microbial
cell walls called lysosome Hemocytes circulate within hemolymph and
carry out phagocytosis, the ingestion and digestion of foreign
substances including bacteria In insects, an exoskeleton made of
chitin forms the first barrier to pathogens
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Copyright 2008 Pearson Education, Inc., publishing as Pearson
Benjamin Cummings Innate Immunity of Vertebrates Innate defenses
include: barrier defenses, phagocytosis, antimicrobial peptides
Additional defenses are unique to vertebrates: the inflammatory
response and natural killer cells The immune system of mammals is
the best understood of the vertebrates
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Benjamin Cummings Barrier Defenses Mucus traps and allows for the
removal of microbes Many body fluids including saliva, mucus, and
tears are hostile to microbes The low pH of skin and the digestive
system prevents growth of microbes Barrier defenses include the
skin and mucous membranes of the respiratory, urinary, and
reproductive tracts
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Copyright 2008 Pearson Education, Inc., publishing as Pearson
Benjamin Cummings Cellular Innate Defenses White blood cells
(leukocytes) engulf pathogens in the body Groups of pathogens are
recognized by Toll- like receptors (TLR)
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Fig. 43-3 Microbes PHAGOCYTIC CELL Vacuole Lysosome containing
enzymes Phagocytosis: (=eating, =cells) engulfing pathogens
Exocytosis cellular debris is released
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Phagocytosis A white blood cell engulfs a microbe, then fuses
with a lysosome to destroy the microbe There are different types of
phagocytic cells: Neutrophils engulf and destroy microbes
Macrophages are part of the lymphatic system and are found
throughout the body Eosinophils discharge destructive enzymes
Dendritic cells stimulate development of acquired immunity
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Cell Types: Red & White
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Fig. 43-8-1 PathogenSplinter Macrophage Mast cell Chemical
signals Capillary Phagocytic cell Red blood cells How your skin
keeps out pathogens Ruptured mast cells (in tissue) release
histamines chemical signal to other phagocytic cells Capillaries
dilate, increase blood flow increase phagocytic cells The clotting
process also starts Platelets Clotting factors signal Fibrin
produced
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Fig. 43-8-2 PathogenSplinter Macrophage Mast cell Chemical
signals Capillary Phagocytic cell Red blood cells Fluid
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Fig. 43-8-3 PathogenSplinter Macrophage Mast cell Chemical
signals Capillary Phagocytic cell Red blood cells Fluid
Phagocytosis More phagocytic cells are released Pathogenic bacteria
are engulfed and destroyed Pus, a fluid rich in white blood cells,
dead microbes, and cell debris, accumulates at the site of
inflammation
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Fig. 43-7 Thymus Lymph nodes Spleen Lymphatic vessels
Lymphocyte maturation White blood cells called lymphocytes
recognize and respond to antigens, foreign molecules Lymphocytes
that mature in the thymus above the heart are called T cells, and
those that mature in bone marrow are called B cells
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Acquired Immunity results from B- and T-cells T-cells Thymus
Combats viruses (intracellular pathogens) B-cells Bone marrow &
spleen Combats bacteria (extracellular pathogens)
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Cell Types: Red & White
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Pathogens have antigens, B-cells have antibodies Antigens: Each
pathogen type has unique surface molecules Antibody binding: Causes
antibodies to be secreted from B-cell Antibodies: Surface proteins
of B- cell Match antigens
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Fig. 43-9 Antigen- binding site Antigen- binding site Antigen-
binding site Disulfide bridge Variable regions Constant regions
Transmembrane region Plasma membrane Light chain Heavy chains T
cell chain chain Disulfide bridge Cytoplasm of T cell (b) T cell
receptor Cytoplasm of B cell (a) B cell receptor B cell V V C C V V
CCCC VV Both B- and T-cells have Antigen binding sites
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Fig. 43-10 Antigen-binding sites Antigen- binding sites
Epitopes (antigenic determinants) Antigen Antibody B Antibody C
Antibody A CC C V V V V C
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Lymphocyte Development The acquired immune system has three
important properties: Receptor diversity A lack of reactivity
against host cells Immunological memory
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A Pathogen is tagged for Attack; a B-cell is selected for
cloning Antibodies cause: Neutralization Agglutination
Precipitation rupture Selection causes rapid clonal replication
Selection Replication
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Fig. 43-14 B cells that differ in antigen specificity Antibody
molecules Antigen receptor Antigen molecules Clone of memory
cellsClone of plasma cells
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The B-cells form Two cell Types: Memory Cells Long-lived Await
future encounters with specific antigen Plasma Cells Secrete many
antibodies to mark and block more bacteria Selection
Replication
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Secondary Immune Response Get a disease, you get natural
immunization e.g. chicken pox Immunization: injecting chemical or
heat inactivated antigens a.k.a vaccination Antibodies to A
Antibodies to B Secondary immune response Primary immune response
Antibody concentration Exposure to antigen A Exposure to antigens A
and B Time (days) 10 4 10 3 10 2 10 1 10 0 0714212835424956
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Fig. 43-15 Antibodies to A Antibodies to B Secondary immune
response to antigen A produces antibodies to A; primary immune
response to antigen B produces antibodies to B. Primary immune
response to antigen A produces antibodies to A. Antibody
concentration (arbitrary units) Exposure to antigen A Exposure to
antigens A and B Time (days) 10 4 10 3 10 2 10 1 10 0
0714212835424956
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Pathogens can evolve to avoid detection Some pathogens change
surface proteins Memory cells can not recognize Pathogens have
shorter generation time relative to host, :. they can evolve faster
What does this mean for the efficacy of any given human-made
antibiotic? Some pathogens like AIDS hide inside your bodys cells
Intracellular invaders are dealt with by T-cells
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Like B-cells, T-cells have Diverse antigen receptors Two types:
Cytotoxic T-cell, Helper T-cell Fig. 43-12 Infected cell Antigen
fragment Class I MHC molecule T cell receptor (a) Antigen
associates with MHC molecule T cell recognizes combination
Cytotoxic T cell(b)Helper T cell T cell receptor Class II MHC
molecule Antigen fragment Antigen- presenting cell Microbe 1 1 1 2
2 2
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Fig. 43-18-1 Cytotoxic T cell Perforin Granzymes TCR CD8 Class
I MHC molecule Target cell Peptide antigen Once bound to CD8
receptor, T-cell becomes an active killer Cytotoxic T-cells
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Fig. 43-18-2 Cytotoxic T cell Perforin Granzymes TCR CD8 Class
I MHC molecule Target cell Peptide antigen Pore Perforins create
pores in surface of target cell Granzymes enter cell initiate
apoptosis (cell death) Cytotoxic T-cells
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Fig. 43-18-3 Cytotoxic T cell Perforin Granzymes TCR CD8 Class
I MHC molecule Target cell Peptide antigen Pore Released cytotoxic
T cell Dying target cell Perforins create pores in surface of
target cell Granzymes initiate apoptosis (cell death) Cytotoxic
T-cells
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Fig. 43-17 Antigen- presenting cell Peptide antigen
Cell-mediated immunity (attack on infected cells) Class II MHC
molecule CD4 TCR (T cell receptor) Helper T cell Humoral immunity
(secretion of antibodies by plasma cells) Cytotoxic T cell
Cytokines B cell Bacterium + ++ +
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Cytotoxic T-cells attack diseased of cancerous cells labeled
with MHCs Normal cells make MHC (Major Histocompatibility Complex)
molecules Abnormal cells like those with viruses make MHCs which
bind to viral proteins Those antigens are presented on the surface
of the infected cell Then detected by cytotoxic T-cells and the
infected cell is destroyed
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Major Histocompatibility Complex Genes have ~100 Alternative
Alleles Each MHC type presents a different type of antigen for
T-cells to recognize as alien Gene polymorphism increases chances
of matching antigens Thus increased MHC diversity = increased
disease resistance One study looked at male selection using old
t-shirts and MHC analysis: females favor males with MHCs which
differ from their own --- why is this adaptive?