1. INNATE AND ADAPTIVE IMMUNITY IMMUNE SYSTEM AND DISEASE

2. MECHANISMS OF PATHOGENICITY Pathogenicity : The ability to cause disease Virulence : The extent of pathogenicity PORTALS OF ENTRY Mucous membranes Skin Blood Respiratory tract Gastrointestinal tract

3. MECHANISMS OF PATHOGENICITY Figure 15.9

4. THE CONCEPT OF IMMUNITY Susceptibility : Lack of resistance to a disease Immunity : Ability to ward off disease Innate immunity : Defenses against any pathogen Adaptive immunity : Immunity, resistance to a specific pathogen

5. AN OVERVIEW OF THE BODY’S DEFENSES Figure 16.1 Innate immunity : Defenses against any pathogen Adaptive immunity : Induced resistance to a specific pathogen

6. PHYSICAL FACTORS Skin Epidermis consists of tightly packed cells with Keratin, a protective protein Figure 16.2 Mucous membranes Mucus : Traps microbes Ciliary escalator : Microbes trapped in mucus are transported away from the lungs

7. CILIARY ESCALATOR Figure 16.4

8. CILIARY ESCALATOR Figure 24.7

9. PHYSICAL FACTORS Lacrimal apparatus : Washes eye Saliva : Washes microbes off Urine : Flows out Vaginal secretions : Flow out

10. CHEMICAL FACTORS Fungistatic fatty acid in sebum Low pH (3–5) of skin Lysozyme in perspiration, tears, saliva, and urine Low pH (1.2–3.0) of gastric juice Low pH (3–5) of vaginal secretions

11. NORMAL MICROBIOTA AND INNATE IMMUNITY Microbial antagonism/competitive exclusion: Normal microbiota compete with pathogens or alter the environment Commensal microbiota: One organism (microbe) benefits and the other (host) is unharmed May be opportunistic pathogens

12. Red Blood CellsTransport O 2 and CO 2 White Blood Cells: NeutrophilsPhagocytosis BasophilesHistamine EosinophilsKill parasites FORMED ELEMENTS IN BLOOD FUNCTION CELL MORPHOLOGY

13. FORMED ELEMENTS IN BLOOD MonocytesPhagocytosis Dendritic cellsPhagocytosis Natural killer cellsDestroy target cells FUNCTION CELL MORPHOLOGY

14. FORMED ELEMENTS IN BLOOD T cellsCell-mediated immunity B cellsProduce antibodies PlateletsBlood clotting FUNCTION CELL MORPHOLOGY

15. Percentage of each type of white cell in a sample of 100 white blood cells Neutrophils60–70% Basophils0.5–1% Eosinophils2–4% Monocytes3–8% Lymphocytes20–25% DIFFERENTIAL WHITE CELL COUNT

16. COMPONENTS OF LYMPHATIC SYSTEM Figure 16.5a

17. THE LYMPHATIC SYSTEM Figure 16.5b–c

18. PHAGOCYTOSIS Phago: From Greek, meaning eat Cyte: From Greek, meaning cell Ingestion of microbes or particles by a cell, performed by phagocytes Figure 16.6 Neutrophils Fixed macrophages Wandering macrophages VIDEO

19. Figure 16.7 PHAGOCYTOSIS

20. INFLAMMATION Acute-phase proteins activated (complement, cytokine, and kinins) Vasodilation (histamine, prostaglandins, and leukotrienes) Redness Swelling ( edema ) Pain Heat

21. THE PROCESS OF INFLAMMATION Figure 16.8a, b

22. PHAGOCYTE MIGRATION AND PHAGOCYTOSIS Figure 16.8c [Insert Animation Inflammation: Overview, Steps.]

23. TISSUE REPAIR Figure 16.8d

24. FEVER Hypothalamus normally set at 37°C Toxins from bacteria trigger the deregulation of the hypothalamus Hypothalamus releases prostaglandins that reset the hypothalamus to a high temperature Body increases rate of metabolism Vasodilation and sweating: Body temperature falls ( crisis )

25. FEVER Advantages Increases transferrins Increases interlukin activity Produces Interferon Disadvantages Tachycardia Acidosis Dehydration 44–46°C fatal

26. EFFECTS OF COMPLEMENT ACTIVATION 1. Opsonization or immune adherence: Enhanced phagocytosis 2. Chemotaxis – Attracting macrophages and neutrophils 3. Cell lysis - Membrane attack complex (cytolysis) 4. Clumping or concentration of foreign agents/cells Figure 16.10 COMPLEMENT VIDEO

27. THE COMPLEMENT SYSTEM Figure 16.9 Complement System Overview Video

28. CLASSICAL COMPLEMENT ACTIVATION Figure 16.12

29. LECTIN PATHWAY OF COMPLEMENT ACTIVATION Figure 16.14

30. INTERFERONS (IFNS) IFN-  and IFN-  : Cause cells to produce antiviral proteins that inhibit viral replication Gamma IFN: Causes neutrophils and macrophages to phagocytize bacteria

31. ANTIVIRAL ACTIONS OF INTERFERONS Figure 16.15

32. AN OVERVIEW OF THE BODY’S DEFENSES Figure 16.1 Innate immunity : Defenses against any pathogen Adaptive immunity : Induced resistance to a specific pathogen

33. IMMUNE CELL TYPES (AGAIN…)

34. THE RESULTS OF Ag-Ab BINDING Figure 17.7

35. AGGLUTINATION Figure 17.7

36. OPSONIZATION Figure 17.7

37. COMPLEMENT FIXATION Figure 17.7

38. ANTIBODY-DEPENDENT CELL-MEDIATED IMMUNITY Figure 17.7

39. NEUTRALIZATION Figure 17.7

40. TYPES OF ADAPTIVE IMMUNITY Naturally acquired active immunity Resulting from infection Naturally acquired passive immunity Transplacental or via colostrum Artificially acquired active immunity Injection of Ag (vaccination) Artificially acquired passive immunity Injection of Ab

41. THE NATURE OF ANTIGENS Antigen (Ag) : A substance that causes the body to produce specific antibodies or sensitized T cells Antibodies (Ab) interact with epitopes or antigenic determinants

42. ANTIGENS Figure 17.1

43. ANTIBODIES Figure 17.3a,b

44. Monomer 80% of serum Abs In blood, lymph, and intestine Cross placenta Enhance phagocytosis; neutralize toxins and viruses; protects fetus and newborn Half-life = 23 days IgG ANTIBODIES

45. Pentamer 5–10% of serum Abs In blood, in lymph, and on B cells Agglutinates microbes; first Ab produced in response to infection Half-life = 5 days IgM ANTIBODIES

46. INNATE VS. ADAPTIVE IMMUNITY

48. IMMUNOLOGICAL MEMORY Antibody titer is the amount of Ab in serum Primary response occurs after initial contact with Ag Secondary (memory or anamnestic) response occurs after second exposure

49. IMMUNE RESPONSES TO REPEAT ANTIGENS Figure 17.16

50. DUAL NATURE OF ADAPTIVE IMMUNITY Figure 17.8

51. Major histocompatibility complex (MHC) expressed on mammalian cells T-dependent antigens (recognized by T cell) Ag presented with (self) MHC to T H cell T H cell produces cytokines that activate the B cell T-independent antigens (does not stimulate T cells) Stimulate the B cell to make Abs ACTIVATION OF B CELLS ADAPTIVE IMMUNE SYSTEM OVERVIEW ANIMATION

52. ACTIVATION OF B CELLS Figure 17.4

53. CLONAL SELECTION Figure 17.5

54. ACTIVATION OF B CELLS B cells differentiate into Antibody-producing plasma cells Memory cells Clonal deletion eliminates harmful B cells

55. ANTIGEN-PRESENTING CELLS Digest antigen Ag fragments on APC surface with MHC B cells Dendritic cells Activated macrophages

57. ACTIVATED MACROPHAGES Figure 17.14

58. T HELPER CELLS CD4 + or T H cells TCRs recognize Ags and MHC II on APC Receptor binding is then a costimulatory signal on APC and T H T H cells produce cytokines and differentiate into T H 1 T H 2 Memory cells

59. ACTIVATION OF CD4 + T HELPER CELLS Figure 17.10

60. T CYTOTOXIC CELLS CD8 + or T C cells Target cells are self carrying endogenous antigens Activated into cytotoxic T lymphocytes (CTLs) CTLs recognize Ag + MHC I Induce apoptosis in target cell CTL releases perforin and granzymes

61. T CYTOTOXIC CELLS Figure 17.11

62. Granular leukocytes destroy cells that don’t express MHC I Kill virus-infected and tumor cells Attack parasites NATURAL KILLER (NK) CELLS

63. ANTIBODY MEDIATED TOXICITY Antibody-dependent cell-mediated cytotoxicity Figure 17.15b

64. Figure 17.15a ANTIBODY MEDIATED TOXICITY

65. CELLS COMMUNICATE VIA CYTOKINES CytokineRepresentative Activity Interleukin-1 (IL-1)Stimulates T H cells in presence of antigens; attracts phagocytes Interleukin-2 (IL-2)Proliferation of antigen-stimulated CD4 + T helper cells, proliferation and differentiation of B cells; activation of CD8 + T cells and NK cells Interleukin-12 (IL-12)Inhibits humoral immunity; activates T H 1 cellular immunity

66. CELLS COMMUNICATE VIA CYTOKINES CytokineRepresentative Activity ChemokinesInduce the migration of leukocytes TNF-αPromotes inflammation Hematopoietic cytokines Influence differentiation of blood stem cells IFN-  and IFN-  Response to viral infection; interfere with protein synthesis IFN-  Stimulates macrophage activity