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Bio 1b – Zoology Hannah Nevins Immunity: the body’s defense system An immune cell (macrophage) engulfs a yeast cell (pathogen)

Dec 22, 2015

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  • Slide 1
  • Bio 1b Zoology Hannah Nevins Immunity: the bodys defense system An immune cell (macrophage) engulfs a yeast cell (pathogen)
  • Slide 2
  • 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
  • Slide 3
  • Copyright 2008 Pearson Education, Inc., publishing as Pearson 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
  • Slide 4
  • 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
  • Slide 5
  • Fig. 43-7 Adenoid Tonsil Lymph nodes Spleen Peyers patches (small intestine) Appendix Lymphatic vessels Lymph node Masses of defensive cells Blood capillary Lymphatic vessel Tissue cells Interstitial fluid Human Lymphatic system
  • Slide 6
  • Copyright 2008 Pearson Education, Inc., publishing as Pearson 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
  • Slide 7
  • 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)
  • Slide 8
  • Fig. 43-3 Microbes PHAGOCYTIC CELL Vacuole Lysosome containing enzymes Phagocytosis: (=eating, =cells) engulfing pathogens Exocytosis cellular debris is released
  • Slide 9
  • 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
  • Slide 10
  • Cell Types: Red & White
  • Slide 11
  • 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
  • Slide 12
  • Fig. 43-8-2 PathogenSplinter Macrophage Mast cell Chemical signals Capillary Phagocytic cell Red blood cells Fluid
  • Slide 13
  • 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
  • Slide 14
  • 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
  • Slide 15
  • Acquired Immunity results from B- and T-cells T-cells Thymus Combats viruses (intracellular pathogens) B-cells Bone marrow & spleen Combats bacteria (extracellular pathogens)
  • Slide 16
  • Cell Types: Red & White
  • Slide 17
  • 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
  • Slide 18
  • 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
  • Slide 19
  • 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
  • Slide 20
  • Lymphocyte Development The acquired immune system has three important properties: Receptor diversity A lack of reactivity against host cells Immunological memory
  • Slide 21
  • 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
  • Slide 22
  • Fig. 43-14 B cells that differ in antigen specificity Antibody molecules Antigen receptor Antigen molecules Clone of memory cellsClone of plasma cells
  • Slide 23
  • 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
  • Slide 24
  • 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
  • Slide 25
  • 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
  • Slide 26
  • 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
  • Slide 27
  • 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
  • Slide 28
  • 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
  • Slide 29
  • 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
  • Slide 30
  • 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
  • Slide 31
  • 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 + ++ +
  • Slide 32
  • 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
  • Slide 33
  • 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?