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Immunity: the body’s defense system An immune cell (macrophage) engulfs a yeast cell (pathogen) Bio 1b – Zoology Hannah Nevins 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 Innate Immunity of Invertebrates • In insects, an exoskeleton made of chitin forms the first barrier to pathogens • 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 Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings Innate Immunity of Vertebrates The immune system of mammals is the best understood of the vertebrates • Innate defenses include: – barrier defenses, phagocytosis, antimicrobial peptides • Additional defenses are unique to vertebrates: the inflammatory response and natural killer cells Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings Human Lymphatic system Interstitial fluid Adenoid Tonsil Blood capillary Lymph nodes Spleen Tissue cells Lymphatic vessel Peyer’s patches (small intestine) Appendix Lymphatic vessels Lymph node Masses of defensive cells Fig. 43-7 Barrier Defenses Barrier defenses include the skin and mucous membranes of the respiratory, urinary, and reproductive tracts • 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 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 Tolllike receptors (TLR) Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings Phagocytosis: Microbes (=eating, =cells) engulfing pathogens PHAGOCYTIC CELL Vacuole Lysosome containing enzymes Exocytosis – cellular debris is released Fig. 43-3 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 Cell Types: Red & White How your skin keeps out pathogens Ruptured mast cells (in Pathogen Splinter Chemical signals Macrophage Mast cell Fig. 43-8-1 increase blood flow increase phagocytic cells Capillary Red blood cells tissue) release histamines chemical signal to other phagocytic cells Capillaries dilate, The clotting process also starts Phagocytic cell Platelets Clotting factors signal Fibrin produced Fig. 43-8-2 Pathogen Splinter Chemical signals Macrophage Fluid Mast cell Capillary Red blood cells Phagocytic cell Fig. 43-8-3 Pathogen Splinter Chemical signals Macrophage Fluid Mast cell Capillary Red blood cells Phagocytosis Phagocytic cell • 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 Thymus Lymphocyte maturation White blood cells called Lymph nodes Spleen Lymphatic vessels 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 Fig. 43-7 Acquired Immunity results from B- and T-cells T-cells B-cells Thymus Bone marrow & spleen Combats viruses Combats bacteria (intracellular pathogens) (extracellular pathogens) Cell Types: Red & White 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 Both B- and T-cells have Antigen binding sites Antigenbinding site Antigenbinding site Antigenbinding site Disulfide bridge C C Light chain Variable regions V V Constant regions C C Transmembrane region Plasma membrane Heavy chains chain chain Disulfide bridge B cell (a) B cell receptor Cytoplasm of B cell Cytoplasm of T cell T cell (b) T cell receptor Fig. 43-9 Antigenbinding sites Epitopes (antigenic determinants) Antigen-binding sites Antibody A C Antigen Antibody C C Antibody B Fig. 43-10 Lymphocyte Development The acquired immune system has three important properties: Receptor diversity A lack of reactivity against host cells Immunological memory A Pathogen is tagged for Attack; a B-cell is “selected for cloning Antibodies cause: Neutralization Selection causes rapid clonal replication Agglutination Precipitation rupture Selection Replication Fig. 43-14 Antigen molecules B cells that differ in antigen specificity Antigen receptor Antibody molecules Clone of memory cells Clone of plasma cells The B-cells form Two cell Types: Memory Cells Plasma Cells Long-lived Secrete many antibodies to mark and block more bacteria Await future encounters with specific antigen Selection Replication Secondary Immune Response Get a disease, you get Immunization: injecting natural immunization chemical or heat inactivated antigens e.g. chicken pox a.k.a vaccination Antibody concentration Primary immune response Secondary immune response 104 103 Antibodies Antibodies to A to B 102 101 1000 7 Exposure to antigen A 14 21 28 35 42 49 56 Exposure to antigens A and B Time (days) Fig. 43-15 Antibody concentration (arbitrary units) Primary immune response to antigen A produces antibodies to A. Secondary immune response to antigen A produces antibodies to A; primary immune response to antigen B produces antibodies to B. 104 103 Antibodies to A 102 Antibodies to B 101 100 0 7 Exposure to antigen A 14 21 28 35 Exposure to antigens A and B Time (days) 42 49 56 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 body’s cells Intracellular invaders are dealt with by T-cells Like B-cells, T-cells have… Diverse antigen receptors Two types: Cytotoxic T-cell, Helper T-cell Infected cell Antigen fragment Class I MHC molecule T cell receptor (a) Microbe Antigenpresenting cell 1 Antigen associates with MHC molecule 1 1 2 2 Cytotoxic T cell 2 T cell recognizes combination (b) Antigen fragment Class II MHC molecule T cell receptor Helper T cell Cytotoxic T-cells Cytotoxic T cell Perforin Granzymes CD8 TCR Once bound to CD8 receptor, T-cell becomes an “active killer” Class I MHC molecule Target cell Peptide antigen Fig. 43-18-1 Cytotoxic T-cells Cytotoxic T cell Perforin Granzymes CD8 TCR Class I MHC molecule Target cell Pore Peptide antigen Perforins – create pores in surface of target cell Granzymes – enter cell initiate apoptosis (cell death) Fig. 43-18-2 Cytotoxic T-cells Released cytotoxic T cell Cytotoxic T cell Perforin Granzymes CD8 TCR Dying target cell Class I MHC molecule Target cell Pore Peptide antigen Perforins – create pores in surface of target cell Granzymes – initiate apoptosis (cell death) Fig. 43-18-3 Fig. 43-17 Antigenpresenting cell Peptide antigen Bacterium Class II MHC molecule CD4 TCR (T cell receptor) Helper T cell Humoral immunity (secretion of antibodies by plasma cells) + Cytokines + B cell + + Cytotoxic T cell Cell-mediated immunity (attack on infected cells) 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 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?