1. Immunity Chapter 23

2. Smallpox Vaccine Before vaccines, smallpox had up to 50% death rates Now smallpox is practically eradicated

3. Immunity Body’s ability to resist and combat diseases Depends on mechanisms that recognize proteins as self or nonself Antigen – Any molecule the body recognizes as nonself and provokes an immune response

4. Evolution of Defenses Innate immunity – Preset responses to nonself cues – Complement, phagocytes Adaptive immunity – Prepares defenses to specific pathogens encountered during an individual’s lifetime – Cytokines, lymphocytes

5. Adaptive and Innate Immunity

6. Three Lines of Defense Physical barriers – exclude pathogens Innate immunity – begins as soon as antigen is detected Adaptive immunity – forms cells that fight infection and prevent later infection

7. White Blood Cells Form in bone marrow Participate in adaptive and innate responses Release cytokines and other cell-to-cell signaling molecules

8. Chemical Weapons

9. neutrophileosinophil mast cellbasophil White Blood Cells

10. T lymphocyteB lymphocyteNK cell White Blood Cells

11. dendritic cell macrophage White Blood Cells

12. Surface Barriers Physical barriers – Intact skin Mechanical barriers – Mucus, cilia, flushing Chemical barriers – Protective secretions, low pH, lysozyme

13. Cilia in Airways

14. Bacterial Invaders

15. Table 23-3, p.385

16. Innate Immune Response Phagocytosis Complement Fever Acute inflammation

17. Complement Many types of circulating proteins Activated by binding to antigen – Triggers reactions that activate more complement Attract phagocytic cells

18. Membrane Attack Complexes antibody activated complement bacterial pathogen lipid bilayer of pathogen Activation Cascade reactions Formation of attack complexes Lysis of target

19. one membrane attack complex (cutaway view) hole in the plasma membrane of an unlucky baterium Fig. 23-6, p.388 lipid bilayer of one kind of pathogen

20. Acute Inflammation Nonspecific response to foreign invasion, tissue damage Destroys invaders, removes debris Symptoms are redness, swelling, warmth, and pain

21. Inflammation Mast cells release histamine Capillaries dilate and leak Complement proteins attack bacteria White cells attack invaders and clean up

22. a Bacteria invade a tissue and directly kill cells or release metabolic products that damage tissue. b Mast cells in tissue release histamines, which then trigger arteriole vasodilation (hence redness and warmth) as well as increased capillary permeability. c Fluid and plasma proteins leak out of capillaries; localized edema (tissue swelling) and pain result. d Complement proteins attack bacteria. Clotting factors wall off inflamed area. e Neutrophils, macrophages, engulf invaders and debris.Some macrophage secretions kill targets, attract more lymphocytes, and call for fever. Fig. 23-7, p.388

23. Fever Temperature up to 39°C (102°F) Enhances immunity, increases rates of enzyme and phagocyte activity Accelerates tissue repair

24. Features of Adaptive Immunity Self/nonself recognition Specificity Diversity Memory

25. Antigens “Nonself” markers on foreign agents and altered body cells such as tumors Trigger division of B and T cells

26. Memory and Effector Cells When a B or T cell is stimulated to divide, it produces 2 cell types Memory cells: set aside for future use Effector cells: engage and destroy the current threat

27. Key Components of Immune Response MHC markers Antigen-presenting cells T cells B cells Natural killer (NK) cells

28. antigen fragments MHC molecule antigen – MHC complex Formation of Antigen–MHC Complex

29. fragments of engulfed antigen MHC marker that the cell already made antigen-MHC complex displayed at surface of plasma membrane Fig. 23-9, p.390

30. Antibody-Mediated Immune Response naive B cells + antigen + complement Cell-Mediated Immune Response antigen-presenting cells naive helper T cells effector helper T cells + memory helper T cells naive cytotoxic T cells effector cytotoxic T cells + memory cytotoxic cells activated B cells effector B cells + memory B cells Fig. 23-10, p.390 Key Interactions

31. Antigen Interception Antigen-presenting T cells are trapped in lymph nodes Macrophages, dendritic cells, and B cells bind, process and present antigen

32. Fig. 23-11a, p.391 TONSILS RIGHT LYMPHATIC DUCT THYMUS GLAND THORACIC DUCT SPLEEN SOME OF THE LYMPH VESSELS SOME OF THE LYMPH NODES BONE MARROW

33. Fig. 23-11b, p.391 arrays of lymphocytes valve (prevents backflow)

34. Antigen Receptors Antibodies – Synthesized by B cells – Bind to one specific antigen Mark pathogen for destruction by phagocytes and complement proteins

35. Antibody Structure Consists of four polypeptide chains Parts of each chain are variable; provide antigen specificity antigen binding site constant region variable region

36. variable region (dark green) of heavy chain binding site for antigen variable region of light chain constant region (bright green) of heavy chain, that includes a hinged region Fig. 23-12a, p.392 binding site for antigen

37. antigen on bacterial cell (not to scale) binding site on one kind of antibody molecule for a specific antigen Fig. 23-12b, p.392

38. Fig. 23-12c, p.392 antigen on virus particle binding site on another kind of antibody molecule For a different antigen

39. Immunoglobins (Igs) Five classes of antibodies – IgG – IgA – IgE – IgM – IgD

40. a As a B cell matures, different segments of antibody-coding genes recombine at random into a final gene sequence. b The final sequence is transcribed into mRNA. c Processing yields a mature mRNA transcript (e.g., introns excised, exons spliced). d mRNA is translated into one of the polypeptide chains of an antibody molecule. Stepped Art Fig. 23-13, p.393 Antigen Receptor Diversity

41. Antibody-Mediated Immune Response B cell responds to one particular extracellular pathogen or toxin Activated B cell forms clones that differentiate into effector and memory cells Effector B cells secrete antibodies that tag antigens for destruction

42. Antibody-Mediated Response

43. antigen Antigen binds only to antibody specific to it on a naive B cell. clonal population of effector B cells Effector B cells secrete antibodies. Fig. 23-15a, p.395 B Cell Division

44. First exposure to antigen provokes a primary immune response. Another exposure to the same antigen provokes secondary response. effector cellsmemory cells naive B cell effector cellsmemory cells Fig. 23-15b, p.395 B Cell Differentiation

45. Fig. 23-15c, p.395 Secondary Immune Response

46. Cell-Mediated Immune Response Cytotoxic T cells target altered body cells that evade antibody-mediated immune response Antigen-presenting dendritic cells activate helper T cells

47. Fig. 23-16, p.396

48. Cell-Mediated Immune Response Helper T cells secrete cytokines – Induce formation of cytotoxic T cells – Proliferate NK cells – Enhance macrophage activity Destroy infected or altered cells

49. cytotoxic T- cell tumor cell Cell-Mediated Immune Response

50. Immunization Process that induces immunity Active immunization: – Vaccination with antigen – Long-lasting immunity Passive immunization: – Purified antibody is injected – Protection is short lived

51. Allergies Immune reaction to harmless proteins (allergens) IgE binds to mast cells, causing inflammatory response Histamine release causes symptoms

52. Anaphylactic Shock Life-threatening allergic reaction Caused by histamine released by many mast cells Airways constrict Blood pressure drops as fluid leaks out of capillaries

53. Autoimmune Disorders Failure of immune system to distinguish between self and nonself – produces antibodies against self Graves’ disease Multiple sclerosis

54. Deficient Immune Responses Primary immune deficiencies – Present from birth Secondary immune deficiencies – Acquired by exposure to agent such as HIV

55. HIV Replication reverse transcriptase core proteins (two layers) integrase viral RNA enters cell reverse transcription of viral RNA host cell viral DNA viral genes are integrated into the host DNA DNA is transcribed viral RNA viral proteins budding viral RNA

56. lipid envelope with proteins viral coat proteins c The viral DNA becomes integrated into host cell’s DNA. a viral RNA enters a T cell. b Viral DNA forms by reverse transcription of viral RNA. f Virus particles that bud from the infected cell may attack a new one. d DNA, including the viral genes, is transcribed viral DNA Viral RNA viral proteins viral RNA viral enzyme (reverse transcriptase) 25-30  m e Some transcripts are new viral RNA, others are translated into proteins. Both self-assemble as new virus particles. Fig. 23-20, p.396 nucleus

57. HIV Infection HIV infects immune system cells – Macrophages, dendritic cells, helper T cells T cells are killed Cytokine IL-4 is released Immune system destroys itself Secondary infections and tumors cause death

58. Table 23-4, p.399

59. HIV Transmission Virus transmitted by – Sex – Infected mothers – Shared needles Not transmitted by causal contact

60. Treatment No cure AZT and other drugs slow disease and increase life span Traditional vaccines do not work Researchers continue to work