Question 1 (worth 6 points): Answer either A or B An argument can be made that immunologic memory is not really necessary. After all, if you survive your first exposure to a pathogen clearly you didn’t need memory to do so, and if you don’t survive then memory couldn’t have helped you anyway, right? This idea is also reflected on a biodiversity level too: there are vast numbers of species; including all plants, insects, and invertebrates, that have no memory component of their anti-microbial defenses (see Table 4- 8). These organisms get along just fine without memory. However, the arguments above do not fully reflect the benefits that humans, mammals, and other animals do derive from having a memory response. Choose either one or the other of the following responses to the argument above and answer the question it poses. Be sure to both answer the question posed in whichever response you choose, and also explain why your answer refutes the idea that memory is not necessary:
- Why would having a stronger, faster memory response provide a distinct benefit even if you already survived your first exposure to a particular pathogen?
- OR B) Why could having a stronger, faster memory response among older individuals who had already been exposed to a particular pathogen indirectly benefit those younger individuals who were being exposed to that pathogen for the first time?
Question 2 (worth 14 points): Answer all sections – A, B, and C Pathogens have evolved many methods for evading detection and elimination by the immune system. Parasitic protozoans of the genus Trypanosoma can cause a very serious disease in humans, known as ‘sleeping sickness’ or ‘trypanosomiases.’ Trypanosomes seek to evade the immune response by periodically changing which gene they use to make their ‘variable surface glycoprotein’ (VSG), which is the major protein that makes up their outer surface. (This process is illustrated in Kuby Immunology Box 17-4.) Answer the following questions about this interaction between Trypanosomes and the immune system.
A) Trypanosomes are extracellular pathogens that usually range in size from between 16-42 micrometers (mM; one micrometer is one-millionth of a meter) in length. In comparison, macrophages are about 24 mM in diameter, neutrophils about 15 mM, and lymphocytes about 10 mM. Most Trypanosomes are too large to be engulfed by phagocytosis or to try getting inside of many types of human cells. Based on this information, what are some other ways that the immune system could effectively attack these parasites? (4 points) Answer all sections – A, B, and C
B) From the perspective of immune memory, explain why the evasion strategy of Trypanosomes works so effectively at allowing the pathogen to persist in the host individual for a long time. How does this strategy disrupt the normal way the immune system seeks to eliminate a pathogen? (5 points)
C) One way to protect against a pathogen is to develop a vaccine that provokes a protective memory response against a pathogen without causing any of the harmful symptoms – but no such vaccine exists for trypanosomiasis. Why not? How does the evasion strategy of Trypanosoma make the effort to develop an effective vaccine so difficult? (5 points)
Question 3 (worth 15 points): Answer all sections – A-E Cholera is serious disease transmitted by drinking water contaminated with Vibrio cholerae bacteria. The harm caused by a cholera infection comes from a protein toxin produced while the V. cholerae bacteria are in the lumen of the intestine. The cholera toxin induces intestinal epithelial cells to begin pumping salt ions (mostly chloride ions; Cl- ) into the intestinal lumen. As salt ion concentration in the intestinal lumen increases, because of the principle of osmosis water from the inside of the body will flow towards this area of higher dissolved particle concentration: the result is massive dehydration and diarrhea, which can be fatal if not treated. V. cholerae reproduces in the intestinal lumen, and then uses the flow of diarrhea in the host to flush itself back out into the environment where it can infect a new host. Answer the following questions about the immune response to a cholera infection (point value for each subquestion is indicated):
A. A typical immune response, as we have learned about it for much of the semester, involves waiting until a microbe crosses over the outer surface of the body – first innate WBCs near the site of infection, then adaptive WBCs in the lymph nodes, become activated and mount a response against the microbe. Why would that NOT be a good strategy for an infection with V. cholerae? (2 points)
B. Why would it be a better option for responding to a cholera infection to have antigen deliberately brought into the body from the intestinal lumen, made available to B cells BIOL 364: Immunology Spring 2022 Take-home exam #3 and processed/presented to T cells in areas of ‘Gut Associated Lymphoid Tissue (GALT)’? (3 points)
C. Why would a typical IgM or IgG antibody response, made by B cells activated in the lymph nodes, not be maximally effective against a cholera infection? (3 points)
D. Cholera toxin is a soluble protein complex that is not actively made in the cells it affects (as a viral protein would be), and V. cholerae never gets inside host cells. Would you need T cell involvement to mount an effective response to cholera infection? Why or why not? (2 points)
E. Describe the sequence of events that would need to occur to mount a protective antibody response after contracting a V. cholerae infection, starting with cholera antigens becoming available for stimulating the naïve adaptive immune system, and ending with the production of antibodies that could attack cholera and its toxin in the lumen of the small intestine. (5 points)
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