A virus has been identified that encodes a protein which inhibits the transporter-associated with antigen processing (TAP). If the virus infects macrophages, the infected cells are most likely to exhibit a reduction in which of the following? Cell surface class I major histocompatibility complex (MHC) proteins а. O b. Cell surface class II major histocompatibility complex (MHC) proteins Ос. Cell surface co-stimulatory proteins O d. Lysosome function е. Proteasome function

A virus has been identified that encodes a protein which inhibits the transporter-associated with antigen processing (TAP). If the virus infects macrophages, the infected cells are most likely to exhibit a reduction in which of the following? Cell surface class I major histocompatibility complex (MHC) proteins а. O b. Cell surface class II major histocompatibility complex (MHC) proteins Ос. Cell surface co-stimulatory proteins O d. Lysosome function е. Proteasome function

Human Heredity: Principles and Issues (MindTap Course List)

11th Edition

ISBN:9781305251052

Author:Michael Cummings

Publisher:Michael Cummings

Chapter17: Genes And The Immune System

Section: Chapter Questions

Problem 13QP: The Adaptive Immune Response Is a Specific Defense Against Infection In cystic fibrosis gene...

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In addition to phagocytosis, neutrophils use a process called NETs. Which one of the following describes this process? Group of answer choices A. NETs is a neutrophil process that activates the complement system of proteins, which destroys pathogens. B. A net-like structure of DNA, histones, lactoferrins, gelatinase, cathepsin G, and myeloperoxidase is secreted at pathogens. Together these chemicals destroy pathogens. C. NETs works when neutrophils secrete major basic proteins onto pathogens, destroying the pathogens' cell membranes. D. NETs are chemicals secreted by neutrophils that trigger the rapid maturation of lymphoid stem cells into lymphocytes.
1. Glycoproteins coat the outside of viruses; in particular they are important in helping HIV dock to our cells and also help the virus evade our immune system. Below is an image of the HIV transmembrane gp120 protein docking to human cd4 cells via the CXCR4 receptor. HIV-gp120 HIV CXCR4 Coreceptor CCR5 Coreceptor CD4 Receptor CD4 Cell a) i) Describe the general chemical interactions that might be involved in protein- protein interactions between the HIV gp120 protein and the human cd4 CXCR4 protein. Hypothesize what type of amino acid R groups you might find on the ii) exterior regions of each of these proteins, iii) and on the membrane bound portion of these proteins. b) The tertiary structure of gp120 is shown below. Please describe the protein (make sure to cover primary, secondary, and tertiary levels).
Human immunodeficiency virus (HIV), the causative agent of acquired immune deficiency syndrome (AIDS) infects T-helper cells that have the CD4 receptor on their surface: gp120 CD4 receptor -CXCR4 coreceptor RNA- Revorse transcriptase enzyme Core with - protein coat Capsomeres of protein coat Envelope T cll DNA (a) Structure of HIV (b) HIV infecting a T cell with CD4 receptors, and CXCR4 coreceptors which are distributed over the surface of the cell Copyright e 2001 Benjamin Cummings, an imprint of Addison Wesloy Longman, Inc. A. As shown in the above diagram, HIV attaches to a susceptible cell by a binding interaction between the gp120 protein on the virus protein and the CD4 and CXCR4 receptors on the surface of the T-helper cell. What will be the next event in the virus life cycle? B. One mechanism for transmission of HIV is direct contact during sexual activity. What is the other common mechanism of transmission?
For many years it was a complete mystery howcytotoxic T cells could see a viral protein that seemed to bepresent only in the nucleus of the virus-infected cell. Theanswer was revealed in a classic paper that took advan-tage of a clone of T cells whose T cell receptor was directedagainst an antigen assoicated with the nuclear protein ofthe 1968 strain of influenza virus. The authors of the paperfound that when they incubated high concentrations ofcertain peptides derived from the viral nuclear protein, thecells became sensitive to lysis by subsequent incubationwith the cytotoxic T cells. Using various peptides from the1968 strain and the 1934 strain (with which the cytotoxic Tcells did not react), the authors defined the particular pep-tide responsible for the T cell response (Figure Q24–1).A. Which part of the viral protein gives rise to thepeptide that is recognized by the clone of cytotoxic T cells? Why do not all viral peptides sensitize the target cells forlysis by the cytotoxic T…
One important role of Fas and Fas ligand is to medi-ate the elimination of tumor cells by killer lymphocytes.In a study of 35 primary lung and colon tumors, half thetumors were found to have amplified and overexpressed agene for a secreted protein that binds to Fas ligand. How doyou suppose that overexpression of this protein might con-tribute to the survival of these tumor cells? Explain yourreasoning.
Experiments are performed to analyze protein tyrosine phosphorylation in response to TCR stimulation. For these experiments, T cells are stimulated with anti-CD3 antibody, and then lysates are prepared and run on a protein (SDS-PAGE) gel to separate the proteins by molecular weight. The proteins are transferred from the gel to a membrane for immunoblotting using an antibody that binds to all phosphorylated tyrosine residues in any protein; this antibody is called ‘anti-phospho-tyrosine antibody,’ and is abbreviated as anti-P-Y. The results are shown in the figure below. You confirm that the mutant T cells express normal levels of all the proteins detected in the WT cells, including PLC-g, SLP-76, ITK, ZAP-70, LCK, LAT, and the CD3 and TCRz proteins. Based on these data, which of the following proteins (biotin, hygromycin, and streptavidin) can rule out its presence? Briefly explain your answer. What protein is most likely defective in the mutant cells and why? For the protein you…
Poliovirus is highly cytopathic both in cultured cells and in animals. Inoculation of mice with poliovirus leads to a robust antibody and cellular response. Explain why mice infected with a poliovirus mutant that cannot cause cell death have poor antibody and cellular responses. What would be one strategy to restore robust antibody and cellular responses in mice infected with this mutant virus?
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The five classes of immunoglobulin differ in …. Select one: a. None of the above b. Ability to bind various classes of antigens (viral, bacterial etc) c. Make up of the heavy and light chains d. Rate of mutation in the variable domain (i.e. speed at which each class can respond to a new antigen) e. Size of the variable domain
Define the following terms: a. tus-ter complex b. chimera c. MHC antigens d. helices e. primer
A mutant B cell line is examined by confocal microscopy after incubation with a microbial pathogen recognized by the BCR on these B cells. The B cells have been stained with antibodies to visualize the localization of polymerized actin and microtubules. As a control, wild-type B cells are examined. The results are shown in the figure below, with the numbers indicating the proportion of cells examined that show each pattern of staining. To identify the specific signaling defect in these mutant B cells, a reasonable biochemical assay would be to: Determine if BCR stimulation of mutant B cells produces enhanced binding of the B cell to the microbe Determine whether the mutant B cells have reduced levels of the enzyme Protein kinase C-q Determine whether the mutant B cells are overexpressing the enzyme Vav Determine whether BCR stimulation of mutant B cells promotes exchange of GDP for GTP on cdc42 Determine whether BCR stimulation of mutant B cells produces increased levels of DAG
The Gram-negative bacterium Yersinia pestis, thecausative agent of the plague, is extremely virulent. Uponinfection, Y. pestis injects a set of effector proteins intomacrophages that suppresses their phagocytic behaviorand also interferes with their innate immune responses.One of the effector proteins, YopJ, acetylates serines andthreonines on various MAP kinases, including the MAPkinase kinase kinase TAK1, which controls a key signalingstep in the innate immune response pathway. To deter-mine how YopJ interferes with TAK1, you transfect humancells with active YopJ (YopJWT) or inactive YopJ (YopJCA)and with FLAG-tagged active TAK1 (TAK1WT) or inactiveTAK1 (TAK1K63W), and assay for total TAK1 and for phos-phorylated TAK1, using antibodies against the FLAG tag oragainst phosphorylated TAK1 (Figure Q23–1). How doesYopJ block the TAK1 signaling pathway? How do you sup-pose the serine/threonine acetylase activity of YopJ mightinterfere with TAK1 activation?