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Practice Exam 2B - Principles of Immunology | BSCI 422, Exams of Immunology

University of MarylandImmunology
Prof. David M. Mosser

Material Type: Exam; Professor: Mosser; Class: PRIN OF IMMUNOLOGY; Subject: Biological Sciences Program; University: University of Maryland; Term: Spring 2011;

Typology: Exams

2010/2011

Uploaded on 10/06/2011

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BSCI 422 Exam 3, Spring 2011
1. _B_ NK cells
a. Generally utilize the adaptor protein DAP16 to inhibit signaling and activation
b. Generally kill cells that are deficient in MHC class I molecule
c. Generally kill cells that are deficient in MHC class II molecule
d. Generally utilize phosphatases to activate cells and induce killing
e. None of the above
2. _C_ The most common order of immune responses to a viral infection is:
a. NK cell killing of infected cells; production of IFN-a; T cell killing of infected cells
b. T cell killing of infected cells; production of IFN-a; NK cell killing of infected cells
c. Production of IFN-a; NK cell killing of infected cells; T cell killing of infected cells
d. All of the above occur with equal frequency
3. _B_ Mutations of which of the following genes would be expected to cause an
immunodeficiency most similar to mutation in TAP1?
a. Complement component C6
b. Perforin
c. RAG2
d. CIITA
e. Mylenoperoxidase
4. _C_ As a precautionary measure, a snake handler gets a shot of horse serum that contains
antibody to snake venom. He has a severe reaction to the horse serum and must be hospitalized
for it. What type of hypersensitivity response is this?
a. Type I
b. Type I
c. Type III
d. Type IV
5. _D_ Which of the following statements about CD28 is false?
a. CD28 is constitutively expressed on all mouse T cells and the majority of human T cells
b. CD28 is a Costimulatory for naïve T cells
c. CD28 is an immunoglobulin superfamily member
d. C28 signals via an ITAM motif
e. None of the above
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BSCI 422 Exam 3, Spring 2011

  1. B NK cells a. Generally utilize the adaptor protein DAP16 to inhibit signaling and activation b. Generally kill cells that are deficient in MHC class I molecule c. Generally kill cells that are deficient in MHC class II molecule d. Generally utilize phosphatases to activate cells and induce killing e. None of the above
  2. C The most common order of immune responses to a viral infection is: a. NK cell killing of infected cells; production of IFN-a; T cell killing of infected cells b. T cell killing of infected cells; production of IFN-a; NK cell killing of infected cells c. Production of IFN-a; NK cell killing of infected cells; T cell killing of infected cells d. All of the above occur with equal frequency
  3. B Mutations of which of the following genes would be expected to cause an immunodeficiency most similar to mutation in TAP1? a. Complement component C b. Perforin c. RAG d. CIITA e. Mylenoperoxidase
  4. C As a precautionary measure, a snake handler gets a shot of horse serum that contains antibody to snake venom. He has a severe reaction to the horse serum and must be hospitalized for it. What type of hypersensitivity response is this? a. Type I b. Type I c. Type III d. Type IV
  5. D Which of the following statements about CD28 is false? a. CD28 is constitutively expressed on all mouse T cells and the majority of human T cells b. CD28 is a Costimulatory for naïve T cells c. CD28 is an immunoglobulin superfamily member d. C28 signals via an ITAM motif e. None of the above
  1. D Above is a schematic of a flow cytometry analysis of SPLEEN cells from an immunodeficiency patient. Deficiency of which of the following would lead to this result? a. CIITA b. Integrin common chain c. Bruton’s tyrosine kinase d. Purine nucleotide phosphorylase e. None of the above For questions 7-12 indicate whether the following is a property of NK cells only (NK), Both (B), CTL only (CTL), or neither (N)
  2. B Perforin in secreted granules contributes to cytotoxicity
  3. NK__ Binding of KIRs to MHC sends an inhibitory signal
  4. CTL__ Differentiation from precursor cell requires interaction with a licensed APC
  5. N_ Requires CD 28 costimulation to kill target cells
  6. B Can secrete IFN-γ after activation
  7. CTL These cells are lacking in B2-microglobulin deficient individuals Name 2 cytokines that are most likely to be made in the lesion of a patient with lepromatous leprosy, and least likely to be found in a patient with tuberculoid leprosy.
  8. IL-4_____
  9. IL-5_______ Name any stress-induced ligand that can initiate NK cell mediated lysis.
  10. MIC- Write a close approximation of the sequence of a typical concensus ITIM
  11. I/VXYXXL

CD 3

IgM 

  1. You are working to develop a gene therapy cure for an immunodeficiency syndrome caused by a defect in Complement factor B. You are using a mouse knockout model that has no expression of any Factor B protein and the gene therapy uses a virus to insert a good copy of the Factor B gene into liver hepatocytes (responsible for generating complement) of adult mice. The reconstituted mice start making functional Factor B, but you discover that they also start producing anti-Factor B antibodies and T cell responses. You never see these (anti-Factor B) immune responses when the same virus is used to insert the factor B gene into normal mice, only in the Factor B knockout mice (though normal mice express increased Factor B levels, indicating that the transgene is working). Explain this phenomenon. a. Though the cells of the knockout mice now produce Factor B, it can still see this gene as foreign and attack it.
  2. Listeria monocytogenes is a bacterium that infects macrophages. It can escape from, the endosome into the cytosol, where it proliferates and uses directed actin polymerization to move into neighboring cells without being exposed to the extracellular environment. Immunocompetent individuals readily control listeria infections. Name one of the main cell types (other than macrophages) and one cytokine you would expect to be involved in this anti- listeria immune response and briefly describe what each does in the control of listeria. a. CTL cells would be activated by infected macrophages and can kill them and the pathogen. b. IL-12 would be involved with the growth and activation of Th1 cells
  3. You are studying the killing of virus-infected B cells by CTL specific for viral peptide. In your assay, you have both virus infected and uninfected B cells, and can distinguish the killing of infected cells from the killing of uninfected cells. You add anti-B7 antibody to the assay. Will killing of infected cells increase, decrease or stay the same? a. B7 has no effect on killing. It only affects proliferation; therefore producing a B antibody wouldn’t help kill infected cells.
  4. As part of your undergraduate research project, you identified a new virus in the laboratory. You found two variants of the same virus that appear to be similar, except one variant grows very rapidly in tissue culture, while the other grows slowly. You inject each variant virus into mice and to your surprise; the rapidly growing virus doesn’t seem to make the mice very sick at all. However, the mice infected with the slow-growing virus get sick and eventually die. Other than the usual “I mixed up the viruses”, how do you explain this phenomenon? a. Slower virus doesn’t inhibit MHC presentation and therefore doesn’t trigger immune response like the fast growing one. This is because a fast growing virus strains the protein machinery of the cell to the point where it cannot make sufficient MHC. Low

MHC then triggers NK cells to not be inhibited and kill the cell that their CD94:NKG2c activating signals bind to.

  1. IL-2 knockout mice have a very mild immune phenotype (in fact, no phenotype was detected until the mice were allowed to get old). However, mice deficient for β or γ chain of the IL-2R were much more severe in their immune phenotypes. Why does an IL-2 knockout have a mild deficiency, but receptor knockouts have more severe phenotypes? a. The lack of IL-2 is mild because there are other IL that have the same function. Receptor knockouts have a severe phenotype because the IL-2 receptor is used by multiple ILs.
  2. An allergic patient is treated with an inhibitor of cellular phosphomethyltransferases (PMT1 or PMT2). What effect would this inhibitor likely have on mast cell degranulation following exposure to an allergen? Why? a. It would prevent degranulation by making the membrane of the mast cell less permeable. This is beacause inhibiting phosphomethyltransferase prevents it from methylating phosphates in the cell membrane, which makes it more permeable
  3. What (mechanistic) role does cAMP play in mast cell degranulation? a. cAMP gives the kinases (PKA/PKC) activation to release the granules by phosphorylating the kinases. These kinases then activate microtubules to pull the granule to the cell surface. Section 4. Matching (2 points each) 33-37. Match the single best lettered process (right) that is most closely associated with the numbered molecules (left) involved in chemotaxis.
  4. G Selectin A. chemotactic for leukocytes
  5. C Integrin B. an inducer of cellular apoptosis
  6. A C5a C. firm cell adhesion to the endothelium
  7. E ICAM-1 D. a ligand for selectins
  8. D Mucin E. a ligand that cellular integrins bind to F. an intracellular cell signaling molecule G. transient cell adhesion to the endothelium H. endothelial cell migration factor 38-42. Match the single best description (right) of the numbered cytokines and chemokines (left).
  9. D TNF-α A. APC derived cytokine that drives differentiation of Th1 cells
  10. E IL-4 B. Antiviral cytokine produced by non-immune cells
  11. H MIP-1α C. Receptor is a heterodimer that contains γ chain
  12. B IFN-β D. Major cytokine responsible for effects of septic/endotoxic shock