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Chapter 24

Chapter 24. The Immune System. Pathogenicity of microbes. Pathogens are microbes that can cause disease. Toxins are small organic molecules or pieces of protein or bacterial cell wall that are released when bacteria die. How do pathogens get in? Adhesion Factors.

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Chapter 24

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  1. Chapter 24 The Immune System

  2. Pathogenicity of microbes • Pathogens are microbes that can cause disease. • Toxins are small organic molecules or pieces of protein or bacterial cell wall that are released when bacteria die.

  3. How do pathogens get in? Adhesion Factors • Adhesion factors allow a pathogen to bind to certain cells. • Viruses have spikes that bind to host cell surfaces. • Invasive mechanisms determine the extent of a disease in the body. • Localized vs. Systemic.

  4. Epidemiology • The study of the factors that influence transmission of diseases in human populations. • Infectious diseases; illnesses caused by pathogens, or their products. • Highly transmissible pathogens (virus, bacterial) are contagious.

  5. Transmission of Diseases

  6. Influenza (the flu)- fever, chills, vomiting, cold symptoms. Influenza or "flu" is an infection of the respiratory tract that can affect millions of people every year. It is highly contagious Viral Diseases

  7. Body Defenses: Overview • Physical barriers: skin & epithelial linings & cilia • Immune defenses – internal • Innate, non-specific, immediate response (min/hrs) • Acquired – attack a specific pathogen (antigen)

  8. Lymphatic System: Overview of Immune Defense Organs & Cells Figure 24-2 ab: Anatomy of the immune system

  9. The Composition of Whole Blood (4-6L in an adult) • The percentage ranges for white blood cells indicate the normal variation seen in a count of 100 white blood cells in a healthy individual.

  10. White Blood Cells (leukocytes) (0.1% of formed elements) • Defend the body against pathogens • Two classes • Granular leukocytes • Neutrophils (polymorphonuclear leukocytes) • Eosinophils • Basophils • Agranular leukocytes • Monocytes • Lymphocytes

  11. Neutrophils • Neutrophils • Acute inflammation • Highly mobile phagocytes • Containing bacteria-killing enzymes • Multi-lobular nucleus

  12. More Granular Leukocytes (granulocytes) • Eosinophils (acidophils) • Stain with an acidic red eosin stain • Attracted to foreign compounds reacted with antibodies • They kill pathogens by releasing substances that kill them. • 2-lobed nucleus

  13. Basophils • Stain with a deep purple or blue basic dye • Migrate to damaged tissue and release their granules • Release histamines. • Inflammatory response; increase capillary permeability.

  14. Agranular Leukocytes (agranulocytes) • Monocytes • Migrate into peripheral tissues • Are precursors to macrophages. • Highly mobile phagocytic cells • Oval, kidney-bean shaped nucleus

  15. Agranular Leukocytes (agranulocytes) • Lymphocytes (specific immunity) • Primary cell of the lymphatic system • T-cells attack foreign cells directly • B-cells produce antibodies that bind foreign particles • NK cells; immunological surveyors. Always remain in circulation. They don’t take up residence in tissues. • Large round, purple staining nucleus.

  16. The immune response. Two types • INNATE IMMUNITY: NON-SPECIFIC • ACQUIRED IMMUNITY: SPECIFIC

  17. Innate Immunity: Phagocytosis & Inflammation • Phagocytosis: Just eat it. • THE PHAGOCYTES • macrophages, neutrophils, NK cells • Engulf and digest recognized "foreign" cells – molecules

  18. Our immune system tags the foreign particles • Opsonins- are the tagging proteins that make unrecognizable particles into “food” for phagocytes.

  19. Innate Immunity: Phagocytosis & Inflammation Figure 24-6: Phagocytosis

  20. Inflammatory Response: hallmark fo the innate immune pathway • 1. acute phase • attract immune cells to the infection site; neutrophils • basophils to produce histamine to flush out the area;edema swollen redness. • 2. produce a physical barrier to retard spread of infection. • 3. promote tissue repair post-infection; not an immune function. • Histamines: from mast cells  swelling, edema, b. v . dilation • Interleukins: • Secreted by macrophages • Stimulate liver production of acute phase proteins (opsonins) • Alter the blood endothelium to ease the passage of WBCs. • Bradykinin: stimulates pain & swelling to draw attention to the wound • Membrane attack complex proteins (25 complement proteins). . .

  21. Inflammatory Response: Cytokines Signal Initiation Figure 24-8: Membrane attack complex

  22. Some complement proteins are “warning proteins” • Interferon is one such warning protein. Virus-infected cells produce this protein which in turn binds to receptors of noninfected cells causing them to prepare for possible attack. interferon Virus infected cell Watch Out guys

  23. Acquired Immunity: LymphocytesB cell and T cells lymphopoiesis

  24. Lymphocytes • Cytotoxic T cells • Attack foreign cells or bodies infected with viruses • Cell-mediated immunity • Regulatory T cells • Helper or suppressor T cells • Regulate and coordinate immune response • Memory T cells • Remain “on reserve”

  25. Lymphocytes Antibody-mediated immunity • B cells • Plasma cells produce antibodies • React to specific antigens • Immunoglobins • Antibody mediated immunity • Memory B cells

  26. Acquired Immunity: Antigen-Specific Responses Figure 24-13: Functions of antibodies

  27. T Lymphocytes: One more detail. . . • Major histocompatability complex (MHC) • These incorporate antigen gragments and present them to the T cells; they come in two flavors: • MHC class I • MHC class II

  28. Non-self proteins Antigen Being Presented To the T-cell. HLA antigens (MHC proteins) Self-proteins.

  29. T Lymphocytes: Cell Mediated Immunity Figure 24-16: T lymphocytes and NK cells

  30. Blood Types: Like Antibodies & antigens will agglutinate • Antigens on RBCs (A, B, AB or none = O) • Antibodies in plasma (anti A, anti B, anti AB) • Rh antigens & antibodies

  31. Blood typing depends on RBC antigens • Presence or absence of specific surface antigens on RBC cell membranes. An antigen is a genetically determined glycoprotein. There are 3 antigens we type for: • A, B, and D (Rh) • Antibodies attack “foreign” surface antigens. YOUR antibodies NEVER attack your antigens.

  32. Blood Type • A person with: • Type A blood • Surface antigen A, anti-B antibodies • Type B blood • Surface antigen B, anti-A antibodies • Type AB blood • Surface antigens A and B, no A or B antibodies • Type O blood • No surface antigens, both anti-A, anti-B antibodies • Rh positive has the Rh surface antigens and no Rh antibodies

  33. Figure 20.4 Blood Typing • The blood type depends on the presence of agglutinogens on RBC surfaces.

  34. Blood Typing

  35. INDUCED IMMUNITY

  36. INDUCED IMMUNITY • ACTIVE IMMUNITY- inject a bit of the antigen (vaccine) and let the body’s immune system make antibodies against it. • IMMUNIZATION

  37. “BOOSTER”

  38. Active Immunity. Dependent upon the presence of memory B and T cells capable of responding to lower antigen doses.

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