1. Chapter 31 Opener

2. Table 31.1 Innate and Adaptive Immune Responses to an Infection

3. Figure 31.1 White Blood Cells

4. Figure 31.2 Innate Immunity

5. Figure 31.2 Innate Immunity

6. In-Text Art, Ch. 31, p. 623 (1)

7. In-Text Art, Ch. 31, p. 623 (2)

8. Figure 31.3 Interactions of Cells and Chemical Signals Result in Inflammation

9. Figure 31.3 Interactions of Cells and Chemical Signals Result in Inflammation

10. Innate vs. adaptive immunity
Concept Animals Use Innate And Adaptive Mechanisms to Defend Themselves against Pathogens
Innate vs. adaptive immunity
Working in pairs and without looking at your notes, identify whether each item below is characteristic of innate immunity and/or adaptive immunity:
1. Barriers such as skin
2. Antibodies
3. Phagocytes
4. Lysozyme
5. B cells
6. Complement system
7. Distinguishing “self” from “non-self”
8. T cells
9. Lymphocytes
10. Interferon
11. Always “ready to go”; does not need time to develop
12. Mucus
13. Found only in vertebrates
14. Can retain a “memory” of previous infections
Answers:
Innate immunity = 1, 3, 4, 6, 10, 11, 12
Adaptive immunity = 2, 3, 5, 7, 8, 9, 13, 14
INSTRUCTOR NOTES:
This exercise can also be done as a “Family Feud” style game, pitting one side of the classroom against the other.
For each question, call on one student from each side of the classroom, and read them the next item on the list. The two students can request assistance from other students on their side of the room (their "family"), but not from the other side. The first student to call out the correct answer gains a point for their side. 10

11. Innate immunity includes a. B cells. b. lymphocytes. c. phagocytes.
Concept Animals Use Innate And Adaptive Mechanisms to Defend Themselves against Pathogens
Innate immunity includes
a. B cells.
b. lymphocytes.
c. phagocytes.
d. Both a and b
e. Both b and c
Answer: c 11

12. Concept 31.2 Innate Defenses Are Nonspecific
Inflammation: helping or hurting?
Working in small groups, review the following common symptoms of inflammation that occur after tissue injury. Identify the proximate cause of each symptom (for example, what exactly causes the injured tissue to become warm, red, etc.). Then discuss whether you think each symptom is adaptive—that is, does the symptom help speed wound healing or help defend against infection?
Heat
Redness
Pain
Swelling
Finally, consider the following question: Many athletes, after an injury, immediately take action to reduce the symptoms of inflammation, with treatments such as compression bandages, ice, aspirin or anti-inflammatory drugs. Given what you have discussed, do you think it is always a good idea to try to reduce symptoms of inflammation after an injury?
Answers:
Heat, redness, and swelling are all due to vasodilation and increased permeability of blood vessels, which in turn are caused by histamine and prostaglandins released by mast cells. The pain is caused partly by the pressure of the swelling, and also by the action of leaked enzymes (from damaged tissues) and prostaglandins on nerve endings.
Most of these symptoms are arguably beneficial. The heat helps accelerate lymphocyte production and phagocytosis, and may directly inhibit growth of pathogens. Swelling helps immobilize the injured tissue, and pain helps prevent further unnecessary motion that might injure it further. Given the possible benefits of inflammation, it is possible that anti-inflammatory drugs may not always be the best course of action and should only be used when truly necessary (e.g., to limit pain, or to limit possible secondary damage when inflammation is occurring in a volume-limited space, such as inside certain complex joints). 12

13. Concept 31.2 Innate Defenses Are Nonspecific
Which of the following statements about inflammation is false?
a. Mast cells release prostaglandins.
b. Dilation of blood vessels causes swelling and heat.
c. Natural killer cells release histamine.
d. Histamine increases the permeability of blood vessels.
e. Aspirin blocks prostaglandin synthesis.
Answer: c
(Mast cells, not natural killer cells, release histamine.) 13

14. Figure 43.7 Immunological memory

15. Figure Vaccination

16. Figure 43.6 Clonal selection

17. Figure 43.10 An overview of the immune responses (Layer 4)

18. In-Text Art, Ch. 31, p. 625

19. In-Text Art, Ch. 31, p. 625

20. Figure 31.4 The Discovery of Specific Immunity

21. Figure 31.4 The Discovery of Specific Immunity

22. Figure 31.4 The Discovery of Specific Immunity (Part 1)

23. Figure 31.4 The Discovery of Specific Immunity (Part 2)

24. Figure 31.5 Clonal Selection in B Cells

25. Figure 31.5 Clonal Selection in B Cells

26. Figure 31.6 The Adaptive Immune System

27. Figure 31.6 The Adaptive Immune System

28. Figure 31.6 The Adaptive Immune System (Part 1)

29. Figure 31.6 The Adaptive Immune System (Part 2)

30. Apply the Concept, Ch. 31, p. 629

31. Concept 31.3 The Adaptive Immune Response Is Specific
Antibody production
Suppose you were exposed to a new cold virus when you walked in to lecture today. Your body has never encountered this particular virus before. The virus is now circulating in your body, and is encountering B and T cells.
Working in pairs or small groups, discuss what would happen to your ability to produce antibodies against this virus if you…
1. have no helper T cells at all? (Assume you still have other types of T cells.)
2. have no B cells at all?
3. have B and T cells, but due to a genetic mutation, your developing B and T cells never rearranged their DNA?
4. cannot produce any memory cells? (That is, suppose all of your activated B cells become plasma cells, and none become memory cells.)
5. have a genetic mutation such that none of your B cells will divide when activated? (Assume the B cells are otherwise normal and functional.)
Which of the above two scenarios will produce the same (or very similar) symptoms? Explain.
Answers:
Lack of helper T cells will mean that an activated B cell will not undergo clonal expansion normally. Some antibodies will still be produced, but not many.
Lack of B cells will mean that no antibodies will be produced at all.
Lack of DNA rearrangement would almost entirely eliminated the lymphocytes’ ability to recognize different antigens. Instead, only a very few antigens could be recognized.
Lack of memory cells will not affect production of antibodies in the initial infection, but will reduce or eliminate immunity to subsequent infections.
Lack of activation of B cells will mean a drastic reduction in the number of antibodies produced during an infection; essentially, one lone B cell will produce antibodies, instead of the millions of identical B cells that would be produced during clonal expansion.
The two most similar scenarios are lack of helper T cells and lack of B cell division. In either case, clonal expansion is eliminated. 31

32. Concept 31.3 The Adaptive Immune Response Is Specific
If no helper T cells are present,
a. antibodies will be produced normally.
b. a few antibodies will be produced, but not as many as normally would be produced.
c. no antibodies will be produced.
d. I don’t know.
Answer: b
(Helper T cells help stimulate clonal expansion of activated B cells. The result is production of many more antibodies [orders of magnitude more] than a single activated B cell could produce on its own.)
[NOTE TO THE INSTRUCTOR: It can be useful to include an “I don't know” choice with clickers, because it can help you discover how many students really haven’t understood the concept at all. Use of this option may depend on whether you assign participation-only points or performance points (or some combination) to clicker questions in your course. If you only assign participation points, it may be useful to leave the “I don't know” choice in the question, as it gives students a penalty-free way of indicating that more time may be needed on this concept.] 32

33. V1-V2-V3-V4-V5-V6…D1-D2-D3-D4-D5-D6
Concept The Adaptive Humoral Immune Response Involves Specific Antibodies
Build your own immunoglobulin!
Suppose you’re a developing lymphocyte. You are about to start randomly shuffling your DNA to build a “supergene” that you will use to make an immunoglobulin chain. You have a chromosome that contains following DNA regions:
V1-V2-V3-V4-V5-V6…D1-D2-D3-D4-D5-D6
Roll the dice to select one of the V regions.
Roll the dice again to select one of the D regions.
Write down your final combination of gene segments (e.g., V3-D2, or whatever it is). You have just spliced these gene segments together! This is the final combination of your immunoglobulin chain.
Review with a friend:
What will you do with your immunoglobulin chain? (Secrete it? Put it in your membrane?) Review the different types of immunoglobulins and their functions.
Real B cells have 100 V genes, 30 D genes, and 6 J genes for heavy chains, and a similar amount of diversity for light chains. How many possible combinations are there of light chain + heavy chain?
INSTRUCTOR NOTES:
This exercise has two parts:
The first part, in which students assemble their “supergenes,” should be done early in the lecture.
In the second part, an assistant pretends to be an invading flu virus, and the class finds out if any B cell (student) will be able to defend the classroom from the flu virus.
This exercise gives students a small taste of the combinatorial math involved generating a huge number of unique Ig chains from just a few DNA segments. It will also help them remember that each developing lymphocyte ends up with just one type of Ig, and that a lymphocyte can only respond to an antigen if the lymphocyte happens to have assembled an immunoglobulin chain (or, in the case of T cells, T cell receptors) that can bind to that particular antigen.
PART I: For the first part of the exercise, bring in a large set of dice for students to use while selecting genes. Each student should select his or her own combination of genes. Ideally there should be about three times more students than the total of all possible combination of genes, so that there will likely be 2 or 3 students with any given combination. There are 36 possibilities in the 6  6 example given above, sufficient for a large lecture class to have a good chance of generating most possibilities. (For small classes of fewer than 48 students, try a different genetic arrangement of two V genes, two D genes, and two J genes, which students can pick by flipping coins.)
Once students have all selected their genes and have put together their final Ig sequences, ask students to compare sequences with their neighbors and see if any immediate neighbors share the same sequence. They can then talk through the questions at the bottom of the slide.
PART II: Later in the class, have an assistant enter the room pretending to be an invading flu virus, wearing a hat (or some other prop) representing an antigenic epitope. The hat should be labeled with a particular combination of Ig genes, such as “V5-D1” - this is the genetic combination of the Ig chain that can bind to that antigen. Ask the class if anybody can make an IgG that will bind to this particular antigen. If any students have the right combination, assign them to play the roles of a B cell, helper T cell, or cytotoxic T cell. (Ideally, at least three students will have the right combination. If necessary, the professor and any TAs can fill any missing roles.) Next, ask the class (as a whole) specifically what these three cell types will do next to save their classmates from doom.
If no students have the right combination, the class is doomed! Tell them that they will all die. Then start the exercise over with a different flu virus antigen.
If time permits, the chain of events involved in activating B and T cells can also be acted out as a role-play exercise in the front of the room. To do this, invite 6 volunteers to come up front to act out the exciting drama of a pathogen invasion. The 6 students should take the parts of:
1) an invading pathogen or pathogens (dropping several antigens around the classroom);
2) a macrophage that ingests a loose antigen from the pathogen, and then presents the antigen to a helper T cell;
3) the helper T cell;
4) a cytotoxic T cell;
5) a B cell that will become a plasma cell; and finally
6) a B cell that will become a memory cell. 33

34. Concept 31.4 The Adaptive Humoral Immune Response Involves Specific Antibodies
Which of the following cell types produces large numbers of antibodies?
a. Helper T (TH) cell
b. Cytotoxic T (TC) cell
c. Plasma cell
d. Memory cell
e. Both a and c
Answer: c 34

35. Which type of cell expresses Class I? Class II?
Concept The Adaptive Cellular Immune Response Involves T Cells and Their Receptors
MHC proteins
Working in pairs, review the differences between Class I MHC proteins and Class II MHC proteins.
Discuss:
Which type of cell expresses Class I? Class II?
What type of antigen is presented on each class?
Which type of T cell will bind?
What will the T cell do?
INSTRUCTOR NOTES:
This exercise is essentially asking students to derive Table 31.2 from the textbook on their own. (With the addition of one more column, for what the T cell will do. This is to remind students of the role of helper T cells vs. cytotoxic T cells.)
Let pairs work on the questions for about 3–5 minutes, and then draw the empty table on the front board and ask students to help fill in the cells as a group. Then compare to the table in the book. 35

36. Which of the following statements is true about Class II MHC proteins?
Concept The Adaptive Cellular Immune Response Involves T Cells and Their Receptors
Which of the following statements is true about Class II MHC proteins?
a. They are found on macrophages.
b. They are used to present intracellular protein fragments.
c. Cytotoxic T cells will bind to them.
d. Once a T cell binds to them, the antigen-presenting cell is destroyed.
e. I don’t know.
Answer: a
(Answers b, c, and d all describe Class I proteins.)
[NOTE TO THE INSTRUCTOR: It can be useful to include an “I don't know” choice with clickers, because it can help you discover how many students really haven’t understood the concept at all. Use of this option may depend on whether you assign participation-only points or performance points (or some combination) to clicker questions in your course. If you only assign participation points, it may be useful to leave the “I don't know” choice in the question, as it gives students a penalty-free way of indicating that more time may be needed on this concept.] 36

37. Figure 31.7 The Structure of an Immunoglobulin

38. Figure 31.7 The Structure of an Immunoglobulin (Part 1)

39. Figure 31.7 The Structure of an Immunoglobulin (Part 2)

40. In-Text Art, Ch. 31, p. 630

41. In-Text Art, Ch. 31, p. 630

42. Figure 31.8 Heavy-Chain Genes

43. Figure 43.16 Effector mechanisms of humoral immunity

44. Figure 43.17 The classical complement pathway, resulting in lysis of a target cell

45. Figure 31.8 Heavy-Chain Genes

46. Figure 31.9 Heavy-Chain Gene Recombination and RNA Splicing

47. Figure 31.9 Heavy-Chain Gene Recombination and RNA Splicing

48. Figure 31.10 A T Cell Receptor

49. Figure 31.10 A T Cell Receptor

50. Figure 31.11 Macrophages Are Antigen-Presenting Cells

51. Figure 31.11 Macrophages Are Antigen-Presenting Cells

52. In-Text Art, Ch. 31, p. 634

53. In-Text Art, Ch. 31, p. 634

54. Table 31.2 The Interaction between T Cells and Antigen-Presenting Cells

55. Figure 31.12 Tregs and Tolerance

56. Figure 31.12 Tregs and Tolerance

57. Figure 43.18 Mast cells, IgE, and the allergic response

58. Figure 31.13 The Course of an HIV Infection

59. Figure 31.13 The Course of an HIV Infection