Immunology
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	Summary questions for Midterm 2 review
	Study Guide II: "Putting it all together & seeing how it works"   Material covered will be from 10/5 through 11/4. Steps to success: Begin using this study guide 10/5 [10/9 is probably more realistic], not the weekend before the exam! Review Vocabulary List 3 and List 4. READ For sample exam questions, see case outside D234. Review self-quizzes 5-7. READ again. Study exercises and questions: 1. What is T cell education? Why is it important? Diagram the sequence a pre-T cell goes through to a mature virgin T cell. Do B cells get educated as well? If so, where? Is the process the same as for T cells? Any differences between B cell and T cell education? 2. Take a look at your chart or map and review antigens, antigen presenting cells [Mí and B cells], MHC, T & B cells. Make a new map area titled "Antigen processing". Draw a diagram of the sequence involved in response to a novel antigen. Make connections from other appropriate areas of your map to the processing sequence. What is MHC restriction? How does this affect antigen processing and presentation? How does it affect response? 3. Give two examples where MHC typing is useful. Why is it important? 4. Review T cell and B cell education. Draw a sequence which extends their journey beyond graduation to virgin T and B cells. After release from "school" where do they go? Discuss the process of "homing". What is involved in homing? Once virgin cells get to where they are going, then what do they do? [Come back here after you complete #5 below.] Following response to antigen, where do the progeny T and B memory cells go? What are some different routes possible, depending on where they started, type of antigen, and so on? How do different subpopulations of memory cells home to their sites? 5. What is "cell signaling"? Differentiate between cell-cell communication and signal transduction. Make a chart of key cytokines involved in immune response and regulation. Diagram source cells and target cells and the cytokines connecting them during signaling. Note the effect on the target cells. 6. Make a summary diagram of a primary immune response. Include antigen recognition and presentation, the cells involved, the cytokines involved, and the response itself: blastogenesis of T and B cells. Link other areas of your map or chart as appropriate. What is "clonal expansion"? Where does it take place? What subpopulations result? To extend your diagram of effector B cells, see #7 below. To extend your diagram of effector T cells, see #8 below. To extend your diagram of memory cells, return to #3 above. 7. How does a secondary immune response differ from a primary immune response? 8. Diagram a humoral response involving B cells. Extend the diagram to follow different roles of antibodies in removing or neutralizing antigen. 9. Diagram a cellular response involving T cells. Extend the diagram to follow different roles of T cell subpopulations in removing or neutralizing antigen. Extend the diagram to follow different roles of T cell subpopulations involved in regulation of response. Make appropriate connections to regulate humoral responses as well as cellular responses. [See #9 below.] 10. Make a chart on immunoregulation. Include as many factors involved as possible. How are antigens involved in immunoregulation? What is the Jerne Network Theory? Diagram immunoglobulins in a Jerne Network. Diagram T cells in a Jerne network. How are genes involved in immunoregulation? What cytokines are involved? What are their effects? 11. What is "tolerance"? How does it occur? Give an example where this is a beneficial outcome. Give an example where it is a harmful outcome. 12. What is affinity "maturation"? How is important in the overall immune response process? How does affinity maturation occur? 13. Summarize C' [complement]. Distinguish between classical and alternate pathways. What components are involved in each pathway? What are the common features of the two pathways? Diagram the terminal sequence. What is the final result? What breakdown products are active and what is the effect of each? How is C' connected to other systems of immune response? How is the complement cascade regulated? 14. What is inflammation? What are the hallmarks of inflammation? What cells are involved? What is their role? [Review your map or charts.] What cytokines are involved? What is their role? [Review your chart.] What is the role of C'? [Review your diagrams on C'.] What is the difference between exogenous pyrogen and endogenous pyrogen? What happens when they are released? What is the difference between acute and chronic inflammation? 15. What are prostaglandins and leukotrienes? How are they produced? What are their effects? 16. Diagram the inflammatory responses to the following situations, including which cell types and chemical mediators are involved, and including the expected outcome: oak sliver in the skin redwood sliver in the skin TB with Mycobacter tuberculosis [contains protective waxy coat] rhinovirus deep knife wound trichinosis infection 17. Give two examples of inhibitors of inflammation. How do they work? Give an example when inhibiting inflammation is beneficial. Give an example when inhibiting inflammation is harmful. [top of page] Summary Questions for Midterm 2 Review 1. You have the following available: Macrophage from an H-2 [a,a] mouse, T cells from an H-2 [a,c] mouse, and B cells from an H-2 [c,c] mouse. If you mix these cells together in vitro, and add antigen, will you get a response of antibody specific against the antigen? If so, explain the process of how this could occur. If not, explain why there would be no response and give examples of what would need to be changed to get a response. 2. Another adoptive transfer game: Mice of H-2 (a/a) strain [homozygous strain at MHC] were sublethally irradiated [All mature lymphocytes were killed; stem cells were unaffected.] In addition, they were thymectomized just prior to irradiation.   After six weeks, the mice were divided into three groups and immunized with specific antigens as shown below. Which group(s) was/were able to mount a humoral response? [If "none", say so.] Why? Group 1: ragweed pollen Group 2: killed Salmonella bacteria Group 3: DNP (hapten)- BSA conjugate Another batch of these mice were divided into three groups and given thymus transplants from fetal mice of other strains as follows: Group 4: thymus from H-2 (a/b) strain Group 5: thymus from H-2 (b/b) strain Group 6: thymus from H-2 (b/c) strain Are any of these groups able to mount a cell mediated response to tumor antigens? If so, which ones(s)? Are any able to mount a humoral response to tumor antigens? If so, which one(s)? For the groups in 'b' which did not respond, state what else needs to be done to fully reconstitute the mice to immunocompetence. Be specific. Some group 6 mice [from above] were fully reconstituted and shown to have both cell mediated and humoral responses. Skin grafts from sibling mice [H-2 a/a] which were not irradiated or thymectomized were transplanted to the backs of the group 6 mice. Will the grafts be accepted or rejected? Why? 3. What would you expect to see clinically in an individual who had a total lack of expressed MHC I antigens? What responses would remain intact? What responses would be affected? Why? What would you expect to see clinically in an individual who had a total lack of expressed MHC II antigens? 4. A monoclonal antibody specific for cholera toxin was injected into mice (group 1) of the same strain as the cells used to make the monoclonal antibody. The resulting antibodies specific for the binding site of the monoclonal antibody were purified and injected into another set of mice (group 2). Later, cholera toxin was injected into both group 1 and group 2 mice. All of the mice in group 1 died, but none of the mice in group 2 died. Explain why. 5. You have been hired for the summer to work in a lab. They are studying receptor-ligand interactions on the surface of cells. You are assigned to work on a newly identified receptor on DTH cells. It binds a cytokine tentatively called IL-72. The structure of IL-72 is known and an analogue has been synthesized which is thought to block the binding of IL-72 to its receptor. Both IL-72 and its analogue are 7.5 kD single chain proteins. In studies involving NK cells, it was shown that IL-72 stimulated migration. If the analogue, at an equal concentration, was added instead, no migration occurred. If the analogue was added first, then IL-72, there was no migration. It is hypothesized that the situation is similar in DTH cells. You set up an in vitro study to test the DTH migration response to IL-72 and its analogue. You use the same model as used for the NK cells: 1000 cells per well with a membrane barrier. Positive migration is scored by cells passing through the barrier to the other side. Below are your results: Experiment 1:  Added to wells: Migration* 10 pg** IL-72/well ++++ 10 pg analogue/well - 10 pg analogue +10 pg IL-72/well ++++ Experiment 2:  Added to wells: Migration* 10 pg** IL-72/well ++++ 25 pg analogue + 10 pg IL-72/well +++ 50 pg analogue +10 pg IL-72/well - * Migration: ++++ = 75-100% cells through barrier +++ = 50-75% ++ = 25-50% + = 10-25% - = 0-10% **pg: picogram = 1/1,000,000,000,000 gram Give two possible explanations why an equal amount of analogue did not block the effects of IL-72 on DTH cells. Does this experiment confirm that the receptor for IL-72 on the DTH cells is identical to the receptor on the NK cells? Why (not)? [top of page]
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 Updated 8/27/04 by thatcher@sonoma.edu