Immunology Exam 2 - Questions and Answers NKG2D is an activating receptor expressed on NK cells, : T cells, and some cytotoxic : T cells. When stressed or... [Show More] infected cells up-regulate receptors that bind to and activate NKG2D molecules, the stressed or infected cells will be killed. This pathway relies on the fact that stressed or infected cells up-regulate: A. All classical MHC class I molecules B. HLA-C molecules that bind KIRs C. MHC class Ib genes such as MICA, MICB, and RAET1 D. Qa-1 and HLA-E molecules that bind leader peptides of other HLA class I molecules E. HLA-G molecules just like those expressed on the fetal-derived cells in the placenta Some CD1 molecules bind to glycosphingolipids, and are recognized by a subset of T cells known as invariant NKT (iNKT) cells. The ability of these T cells to recognize different glycolipid constituents from microorganisms when they are bound to CD1d places these cells in the 'innate immune' category. While iNKT cells do express a fully rearranged : T-cell receptor, one key feature of the T-cell receptors expressed oniNKT cells also places them in the 'innate immune' category. This feature is: A. iNKT cells have a highly restricted T-cell receptor repertoire, with the majority of cells utilizing the same V and J rearrangement. B. iNKT cells express receptors that are also expressed on NK cells. C. iNKT cells express T-cell receptors that induce inhibitory, rather than activating signals. D. iNKT cells do not generally express CD4 or CD8. E. The T-cell receptors expressed on iNKT cells recognize both MHC class I and MHC class II molecules. T cells expressing : T-cell receptors have been found to recognize a diversity of ligands, including pathogen-derived proteins, self-peptides, and stress-induced molecules. This pattern of antigen recognition shows similarity to that of iNKT cells and MAIT cells, suggesting that : T cells: A. Do not play an important role in immunity, but likely have a non-immune function B. Share features of both innate and adaptive immune cells C. Are only able to respond when the host is infected with a virus such as herpes simplex virus D. Are involved in maintaining the integrity of endothelial cells in the host E. Are most important in responses to tumor cells that show stress responses An important transcription factor activated by antigen receptor signaling in lymphocytes is an NFB heterodimer of the two subunits, p50 and p65Rel. Defects in the IB-kinase complex (NEMO) or mutations in IB that prevent its phosphorylation interfere with NFB activation and result in severe immunodeficiency diseases. This is due to the important function of: A. NEMO in targeting p50:p65Rel for ubiquitination and degradation B. NEMO in ubiquitinating IB causing its release from NFB C. IB in blocking the DNA binding activity of NFB D. IB as a chaperone to promote NFB nuclear localization E. NEMO in phosphorylating IB inducing its degradation, thereby releasing NFB Lymphocyte activation leads to robust proliferation and effector cell differentiation. The metabolic demands of these processes are met, in part, by up-regulation of glycolytic enzymes and nutrient transporters on the activated cell membrane. A key intermediate in the signaling pathway leading to enhanced glucose metabolism following antigen receptor stimulation is: A. The lipid mediator diacyl-glycerol (DAG) B. The phosphoinositide, PIP3 C. Increases in cytoplasmic Ca2+ D. Cleavage of the membrane phospholipid, PIP2 E. The mitochondrial protein, Bcl-2 B. The phosphoinositide, PIP3 The immunosuppressive drug rapamycin acts by inhibiting mTOR. When activated T cells are treated with rapamycin in a cell culture assay, they show greatly diminished proliferation, and accumulate to much lower numbers than control-treated cells. This is because: A. Rapamycin inhibits cells from increasing their synthesis of lipids and proteins. B. Rapamycin inhibits cells from activating the pro-survival protein, Bcl-2. C. Rapamycin inhibits DNA synthesis in activated T cells. D. Rapamycin inhibits cell cycle progression in activated T cells. E. Rapamycin inhibits the T cell's production of the growth factor, IL-2.25. The integrin LFA-1 is constitutively expressed on the surface of restingT cells. Yet, integrin-dependent T cell adhesion to antigen-presenting cells increases substantially following TCR stimulation. This increased integrin-dependent adhesion is mediated in part by: A. Increased synthesis of the LFA-1 protein B. Increased transport of intracellular pools of LFA-1 to the cell surface C. LFA-1 conversion to a high affinity binding state D. Increased phosphorylation of the LFA-1 cytoplasmic tail E. Activation of cdc42 and WASp Humans with defective expression of the integrin LFA-1 have an immunodeficiency disease characterized by the failure of lymphocytes and granulocytes to migrate to tissues at sites of infection or inflammation. A similar immunodeficiency would be expected if individuals had mutations disrupting the gene for: [Show Less]
