Sarah Tonin suffers from chronic urticaria (hives). Hives are an example of Type I (IgE-related) hypersensitivity, and can be caused by an allergic reaction. Ms. Tonin was tested for many common allergens and her IgE was also checked for reactivity with common allergens, but these tests were all negative. However, Ms. Tonin was found to have autoantibodies to her own Fc-epsilon receptors. EXPLAIN to Ms. Tonin why her mast cells are degranulating.
Infected DCs are able to present viral antigens on MHC-I. EXPLAIN TWO ways that uninfected DCs might also be able to present viral antigens on MHC-I to activate naïve CD8+ T-Cells.
Larry is a CD40L knockout, Curley is a CD40 knockout and Moe is an AID knockout. Who is worse off? EXPLAIN
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If you want to get a really good immune response to an antigen, you mix it with necrotic tissue and inject it. Why is necrotic tissue such a good adjuvant?
A prophylactic vaccine for human papillomaviruses (HPV) associated with cancer was licensed in 2006. The vaccine contains antigens of HPV6, HPV11, HPV16, and HPV18. Consider the following hypothetical results of the incidence of cervical cancer carried out in the future. No knowledge of HPV immunization status of the study participants is needed to answer the questions.
In 2020, the CDC collected 500 cervix samples from women 50+ years of age with cervical cancer, and from 500 women without cervical disease. All samples were tested for HPV. Within the cervical cancer cases, HPV was detected as follows: HPV16, 185 cases; HPV18, 60 cases; HPV51, 20 cases. In control women, HPV was detected as follows: HPV16, 20 controls; HPV18, 8 controls; HPV51, 6 controls.
In 2060, CDC again collected 500 cervix samples from women 50+ years of age. All samples were tested for HPV. Within the cervical cancer cases, HPV was detected as follows: HPV16, 30 cases; HPV18, 40 cases; HPV51, 220 cases. In control women, HPV was detected as follows: HPV16, 2 controls; HPV18, 6 controls; HPV51, 18 controls.
What was the effect of the HPV vaccine on cervical cancer caused by HPV16 in the interval between 2020 and 2060?
What happened to prevalence of HPV16 in the population?
What was the effect of the HPV vaccine on cervical cancer caused by HPV18 in the interval between 2020 and 2060?
What happened to prevalence of HPV18 in the population?
Based on these data, which of the following would be your recommendation (circle one): 1. Modify the existing HPV vaccine to include HPV51. 2. Continue with the existing HPV vaccine. EXPLAIN
5A. Myelin Basic Protein (MBP) is a myelin sheath protein ordinarily sequestered from the immune system. Injecting myelin basic protein (MBP) with adjuvant into a mouse induces an autoimmune condition reminiscent of Multiple Sclerosis (MS) called experimental autoimmune encephalomyelitis (EAE). EAE has been used as a model for testing potential drugs to treat multiple sclerosis.
In EAE, the mouse’s immune system attacks MBP in myelin sheaths, but also attacks other sequestered proteins in the myelin sheath (for example, Myelin Proteolipid Protein and Myelin Oligodendrocyte Glycoprotein) even though the mouse was not immunized with them. Why are these other antigens attacked?
5B. If you first feed a mouse MBP for a few weeks, and then inject it with MBP and adjuvant, that mouse won’t get EAE.
Itchy and Scratchy are two syngeneic mice. Suppose you fed Itchy MBP, but fed Scratchy just ordinary chow for a few weeks. What specifically could you adoptively transfer from Scratchy to Itchy to protect Itchy from developing EAE when you inject Scratchy with MBP in adjuvant?
7A. Dr. Rhoda Letter immunized a mouse with purified CD28, prepared splenocytes, fused them with myeloma cells and isolated a hybridoma that made a monoclonal antibody specific for CD28. Dr. Letter purified a quantity of the monoclonal antibody. She wanted to prepare a polyclonal anti-idiotypic antibody to her anti-CD28 monoclonal antibody. To do that, she should immunize which of the following with the monoclonal antibody? a) a mouse genetically identical to the mouse from which she used to prepare the original monoclonal antibody; b) an allogeneic mouse; c) a rabbit; d) a syngeneic mouse except for the MHC-region. EXPLAIN
7B. Circle all the correct responses: The anti-idiotypic antibody might bind to the following: a) CD28; b) B7; c) CTLA-4; d) the original monoclonal antibody
e) none of the above EXPLAIN
For decades, Steven A. Rosenberg at the National Cancer Institute has led clinical cancer trials using a technique of isolating TILs (Tumor-Infiltrating Lymphocytes) from a patient’s tumor, growing the TILs for weeks in tissue culture to high numbers, and then infusing them back into the patient.
8A. EXPLAIN what made him think this would help.
See the first page of a paper published in this week’s Science, attached at the back. Before you read from it, here are a few background facts.
*KRAS is a proto-oncogene, and KRASG12D is an activating mutation in KRAS. *Somatic KRAS mutations are found at high rates in leukemias, colon cancer, pancreatic cancer and lung cancer.
*Human Leukocyte Antigen C*08:02 is an allele of MHC-I (HLA-C).
*A neo-epitope is an epitope generated by a somatic mutation in a cancer cell.
Then, read the first long paragraph of the paper (“Genetic Aberrations”) up to the next paragraph (“To this end”). You can read more if you want to, but it’s not necessary.
8B. There are two categories of mutations in cancer cells: “Driver” mutations, which contribute the cancer cell’s oncogenicity, and “Passenger” mutations, that are just there as a result of the cancer’s genetic instability. Although 9 out of 10 patients had T-Cells specific for neo-epitopes expressed by their own tumors, no two patients had T-Cells that recognized the same neo-epitopes. Were most of these mutations Driver, or Passenger, do you think, and why do you think so?
8C. Three of the 10 patients carried the KRAS mutation, but only 1 of them had T-Cells that were specific for this neo-epitope. What might be the difference between the one who did and the two who didn’t?
8D. Gastrointestinal cancers generally generate fewer neo-antigens than melanomas do. Which tumor type do you think responds better to treatment with checkpoint inhibitors (like anti-CTLA-4)? Based on this paper’s finding, EXPLAIN what approach might make checkpoint inhibitors work better for the one that responds poorly.