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Immunity Pogil Packet Key 4 - 8 P

AP BIO ANSWER KEYS

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Elaine
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67% found this document useful (3 votes)
22K views

Immunity Pogil Packet Key 4 - 8 P

AP BIO ANSWER KEYS

Uploaded by

Elaine
Copyright
© © All Rights Reserved
Available Formats
Download as PDF or read online on Scribd
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9. Becells are a third type of white blood cell that is involved in immunity. a, Draw the symbol that represents a B-cell in Model 2. +b. What is the name of the immune system response that involves B-cells? Humoral response. 10, According to Model 2, are all B-cells the same? Justify your answer with specific evidence from Model 2. No, the ends ofthe surface proteins are different on different Becells. 11. In diagram 2 of Model 2, binding occurs between an antigen and a B-cell. How is this incerac- tion different from the binding that occurs between antigens and helper T-cells? In Model 2, the Becell is binding to an antigen that is still part of the whole pathogen organism. In Model 1, the T-cell did not bind to the antigen until after it had been broken down in the phagocyte and presented on the surface of the phagocyte. 12. Consider diagrams 3~5 in Model 2. Write descriptions similar to those in Question 5 for each of these steps in che humoral response. See Model 2. 13. Isa B-cell an antigen-presenting cell? Justify your reasoning, Yes, the Beell isan APC because it presents the antigen on its surface ina very similar manner to the phagocyte. 14, According to Model 2, do B-cells ever interact with pathogens that have infected a cell? Justify your seasoning with specific evidence from Model 2. No, the B-cells interact with the pathogen directly when it is free inthe blood. 15. Predict what would happen if a B-cell like the one shown in diagram 5 of Model 2 were to run into a helper’T-cell like the ones in Model 1. Since the antigen is presented on the surface ofthe Becell,a helper T-cell could bind to the Becell. Model 3 - Adaptive Immunity Pathogen, * eo 16. Label the following items in Model 3 Pathogen B-Cell Helper T-cell See Model 3 17. Describe the interaction between the B-cell and the helper T-cell in Model 3. The helper T-cell is bound to the B-cell atthe site where the antigen is presented on the B-cells surface. ae when a Belli acivaced by the inceraction with a helper T-cell it begins to produce and dis- perse antibodies. 44, Draw the symbol that represents an antibody in Model 3. x 4. According to Model 3, what does the antibody do to pathogens? The antibody binds to the free pathogens in the blood and forms clumps. 19. How might the interaction between the antibody and pathogens affect the pathogen’ ability o infect its host? The clumping of the pathogens by the antibody would make it dificult for the pathogens to enter the cells ofthe organism and cause an infection Read This! ‘After the B-cell is activated by the helper T-cell, the B-cell enters a phase of rapid cell division. Some of the daughter cells become plasma cells that male even more antibody molecules, some reaching a rate of 2,000 molecules pet second. The other daughter cells become memory B-cells that will scay in the body for several years, ready to respond to the pathogen ifit should ever enter the body again. Model 4 — Immune Response to a Pathogen 20, 21. 22, Br =o 3 ie zo 3a Jao) jive Eacoumer wi the wo. [Pathogen Second Encounter ‘Time Jevith che Same Pathogen “What does the y-axis of the graph in Model 4 represent? The amount of the antibody in the blood. How many times did the organism in Model 4 encounter the same pathogen? Twice. Using Model 4, compare the amount of the antibody generated by the B-cells after the itst encounter with the antigen to the amount of the antibody generated in the second encounter with the antigen. The first encounter does not create much of the antibody. The second encounter produces a lot more of the antibody. Refer co Model 4 4. Compare the time needed to reach the peale amount of antibody production for the frst and second encounters. Peak antibody production was reached sooner the second time the organism was exposed to the pathogen. }. How does your answer to part explain the fact that we get sick the first time we encounter a virus, bue we do not get sick the second time we encounter the same virus? Ie takes longer 10 reach the peak of antibody production following the frst encounter with an anti- gen, fit takes our body several days to make enough antibodies to fight off a virus the first time, we will be sick from the virus during that time, During the second infection. though, our body releases a huge amount of ansibodies almast immediately, effectively defeating the virus before we experi- cence symptoms of being sick 24, People who are allergic to bee stings are actually having a response to the antibodies produced by their immune system when they are stung, This is called anaphylaxis. Most people who end up having a bee sting allergy did not have anaphylaxis the first time they were stung. It is only upon the second sting, or subsequent stings that they have an allergic response. Use what you have learned in this activiy to explain this phenomenon. The firs time the person gets stung by a bee, a small amount of antibody is made over a long period af time. If they have a reaction to the sting it would be minor. Upon getting stung again however, a. much more rapid immune response will occur. Many more antibadies are made in a much shorter amount of time. This causes anaphylaxis. Fass. considerll he diferent types of cells mentioned in this activity that participate in the immune response. Which cells are responsible for the response to the second pathogen exposure illustrated in Model 4 Justify your reasoning. The memory T, cells and he memory B-cells stay in the body for several years. Those are the cells that are responsible forthe quick immune response on the second pathogen exposure. Those cells “remember” the pathogen and are prepared to fight it 26. Consider Models 1 and 2, and the interaction that helper T-cells and B-cells have with the pathogen. 4. Why is the process in Model | called a “cell mediated” response? Helper T-cells will only be activated when the antigen is presented on an APC. They cannot re- spond t0 the free pathogen in the blood. 4. Why is the process in Model 2 called a “humoral” response? Note: Blood was once referred to as one of the humors of the body. Becells respond to the free pashogens in the blood. Extension Questions 27. Consider the life cycle ofa cell. When the memory cells of the immune system ate not activated or responding to a pathogen exposure, what phase of the cell cycle are they likely in? Justify your reasoning, They are likely in the G, phase ofthe cell cycle, meaning they are not dividing or preparing to divide. Read This! Edward Jenner, an English country doctor, is credited with giving the first relatively safe vaccine, He no- ticed that girls who milled cows developed sores on their hands that were similar to the sores of smallpox victims. These sores were called cowpox, but the gis did noc seem to be sick and they did not become ill with the dreaded human disease, smallpox. Legend states that Jenner purposely infected a young boy with serapings from cowpox sores and then exposed the boy to smallpox. The boy did not become ill, and the practice of vaccinations moved rapidly into mainstream medicine. The word vaccination comes from the Latin word for cow, vacca. Today, thanks to intensive vaccination practices in the last half of the 20ch century, smallpox is no longer a dreaded human disease, Since then, vaccines for other diseases like polio and measles have been developed, and we no longer have widespread deaths from these diseases. 28, Use what you learned in this activity to explain why the girls observed by Jenner did not get sick from smallpox. Somchow, being exposed to cowpox led to the creation of antibodies and memory B-cells that ree- ognized smallpox viruses as well. This allowed the milkmaids' immune system to rapidly respond to smallpox, keeping them healthy 29. Using the information from this activity and the Read This! box, waite a definition for the term vaccine, using the terms antigen, antibody, and memory B-cells A vaccine isa way t0 purposely expose a person (or the immune system) to an antigen or pathogen in a safe way so that the immune syste matkes memory B-cells hat will produce antigen-specific antibodies 10 protect against another encounter with the pathogen 30. The common cold is a viral disease. So is AIDS, which is caused by the Human Immunode- ficiency Virus, or HIV. Effective vaccines against these viral diseases have not been developed despite years of research and work by dedicated scientists. One reason for this is the rapid muta~ tion rate of these viruses, leading to new surface proteins in a very short time. Return to Model 2 +o speculate about how this rapid change in the cold virus and HIV make vaccinations difficult 0 develop. The vinal antigens are different with each generation of the virus, so the immune system must go through the entire response process from scratch with each new infection by these viruses. Thus, the memory B-cells are of no wie, because the virus is different each time, 31. Propose a reason why you must get vaccine “booster” shots every few years. The memory T,-cells and the memory B-cells do nor last forever in the body. A booster shot exposes the body once again so there is a slight immnuane response, which increases the number of memory cells in the body and keeps the immunity strong.

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