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Pierce College
Putman/Biol 242
Lecture Unit 04 SGOs: Immunology
Readings: Marieb & Hoehn, Ch. 21
Pierce College Student Outcomes:
Lecture Outcome 3: Differentiate between non-specific resistance mechanisms and specific antibody-mediated
(humoral) immune response and cell-mediated immune response.
By studying lecture notes and the assigned readings, do the following:
1. State what immunity is.
2. List and characterize the two types of immunity. Which is specific with regards to antigen?
Which imparts system-wide immunity? Which is long-lasting and which is short-lived?
3. Describe how physical and physiological barriers contribute to innate immunity.
4. List six cellular and chemical innate immunity mechanisms and describe how each works.
5. What are the two most active phagocytic cells of innate immunity?
6. Describe the mechanism of phagocytosis. What two things must first happen for a phagocyte
to successfully phagocytize a non-self antigen? How do phagocytes kill microbes?
7. What do phagocytes do if target microbes are too big to ingest?
8. What are the effects inflammation? What causes these effects?
9. What are five benefits of inflammation?
10. What factors trigger inflammation?
11. Why might a low-grade fever to beneficial to innate immunity?
12. What are seven compounds released during the inflammation process? What is the source
and effect of each?
13. What processes during inflammation cause edema?
14. Which compounds cause edema during inflammation?
15. During inflammation, which compound triggers the rapid release of neutrophils?
16. Which compounds cause cytotaxis of neutrophils and macrophages during inflammation?
17. Which compound makes free nerve endings more sensitive to pain during inflammation?
18. Aspirin blocks the synthesis of which inflammatory compound?
19. Which inflammatory compound induces fever?
20. What causes pain during inflammation?
21. How are pathogens isolated during the inflammation process?
22. Where do interferons come from? What do they do? How might an interferon produced in
response to an influenza virus help innate immunity combat other types of viruses? Do
interferons help cells that are already infected with a virus?
23. What is complement? What two factors activate complement? What are three effects of an
activated complement cascade?
24. What are antigens? In your body, where might antigens be found? What kinds of cells have
“self” antigens? What are “non-self” antigens? What are gamma-globulins?
25. What attaches to antigens?
26. How can several different antibodies attach to a single antigen?
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27. Explain how several helper T-cells, each with different antigenic receptors, might attach to
the same type of antigen on a virus?
28. What are MHCs? Are the two classes of MHCs? What kinds of cells exhibit each class of
MHCs? How is it that MHCs are really “double antigen” complexes? Where is the second
antigen in an MHC? What is its source?
29. Describe the initial step of acquired immunity. What three cell types are involved? Where are
they found? What are APCs? What triggers the formation of APCs? What is the source of
interleukin 1? What triggers the secretion of interleukin 1?
30. Where are helper T-cell formed? Where do they mature? What kind of receptors do helper Tcells have? How do the many types of helper T-cells differ?
31. What kinds of cells have class I MHCs? Class II MHCs? CD4 receptors? CD8 receptors?
Into what do CD4 and CD8 fit?
32. What stimulates the binding of APCs to helper T-cells?
33. In the cell mediated process, what stimulates the secretion of interleukin 2? What cell
secretes interleukin 2?
34. What kind of helper T-cells are involved in the cell mediated process? What activates these
cells? When they’re activated, they do what?
35. What types of cells are activated by interleukin 2?
36. Compare and contrast cytotoxic T-cells and natural killer cells regarding their structure, what
they bond to and method(s) of attack.
37. What two types of antigens are required for a cytotoxic T-lymphocyte to bond onto an
infected cell? What kind of receptors do cytotoxic T-cells have? Can cytotoxic T-cells bind
onto APCs? Normal body cells? Abnormal (infected) body cells? Why or why not in each
case!
38. What two things are required to activate a cytotoxic T-cell? What happens when a cytotoxic
T-cell is activated?
39. What is the killing mechanism employed by cytotoxic T-cells? What is the function of
perforin? What ion activates it? What are grandzymes?
40. Why are natural killer cells classified as being part of both innate immunity and acquired
immunity? What activates natural killer cells? (What are these cells constantly looking for?)
What kinds of cells do natural killer cells attack? Why? What is their mechanism of attack?
41. What is the first step of humoral immunity? Where are B-lymphocytes formed? Where do Bcells mature? What kind of receptors do B-cells have? How do the many types of B-cells
differ? What is the difference between the activation of helper T-cells and B-cells?
42. After a B-cell encounters an antigen, how does the antigen get into the B-cell’s MHC
complexes? What kind of MHC complex(es) do B-cells have?
43. In humoral immunity, what specifically do activated B-cells bind to? Which interleukin
stimulates B-cell binding?
44. In humoral immunity, what do helper T-cells bind to? Must they be activated first? What
activates helper T-cells?
45. What two factors stimulate the differentiation and proliferation of B-cells? Into what do Bcells differentiate and proliferate? Activated B-cells are called what? What do these cells
secrete? What are these substances specific for?
46. What stimulates the secretion of antibodies? What cells produce antibodies?
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47. Are antibodies removed from the blood in urine? Why or why not?
48. Why can antibodies attach to antigens on pathogens in blood or lymph but not to antigens on
pathogens in solid tissues?
49. From what two sources can antibodies be passively obtained? Why are breast-fed babies
healthier (less sick) than formula-fed babies?
50. How can antibodies be actively obtained?
51. Can any antibody attach to any antigen? Why or why not?
52. What are four functions of antibodies? What is opsonization?
53. What are monoclonal antibodies? How are they produced? What are they used for?
54. What happens to activated helper T-cells and B-cells when antigen concentrations drop
below a certain, low level? What is the advantage in the development of a few memory cells?
55. What do interleuken 1, interleukin 2 and interleukin 4 stimulate? What is the source of each?
56. Explain fully the events of acquired immunity starting from the appearance of antigen.
Include all of the cell types involved as well as the source and effects of the major cytokines.
57. What is the difference between active and passive immunity? Which stimulates immune
memory? What is the mechanism behind naturally-acquired active immunity (two words)?
Explain fully the mechanism behind artificially-acquired active immunity!
58. Why is it not possible for a person to contract influenza from a properly-prepared influenza
vaccine? If a person DOES contract influenza after a properly-prepared influenza vaccine,
what happened? Why should people who are allergic to eggs be careful about receiving
vaccines?
59. What are two sources of naturally-acquired passive immunity?
60. What are the uses of artifically-acquired passive immunity? Does passive immunity stimulate
immune memory?
61. Are the causes of autoimmune diseases fairly well known? What happens in autoimmune
diseases?
62. What are the major symptoms of lupus? What causes these symptoms?
63. Besides lupus, what are four other autoimmune diseases mentioned in lecture?
64. Which virus causes AIDS? What is its closest relative?
65. Which cell types does HIV attack? What type of receptor does it bond to? Which
glycoprotein complexes on the coat of HIV bonds to these receptors?
66. What kind of genetic material does HIV have? What does reverse transcriptase do?
67. What overall effect does the HIV virus have on the immune system? Why?
68. What does it mean to be HIV positive?
69. Where do HIV viruses tend to concentrate?
70. How do the three drug classes mentioned in lecture work against HIV?
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