Becker's World of the Cell (9th Edition)
9th Edition
ISBN: 9780321934925
Author: Jeff Hardin, Gregory Paul Bertoni
Publisher: PEARSON
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Chapter 18, Problem 18.3CC
The autoimmune disease systemic lupus erythematosus can arise when a patient’s own immune system attacks snRNPs. Why would attacking these complexes lead to such devastating effects?
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Toll-like receptors represent an ancient pathogen-recognition system. The first pattern recognition receptor (PRR) important in innate immune responses was discovered in the fruit fly Drosophila melanogaster. Stimulation of this receptor, called Toll, induces:
The synthesis of prostaglandins and leukotrienes
The inflammatory response in Drosophila hemolymph vessels
The production of antimicrobial peptides
The recruitment of phagocytic cells to the site of infection
The activation of Drosophila complement
TRUE OR FALSE: In most cases where certain viral infections appears to be linked to an autoimmune disease, there is often a very clear indication of cross-reactive antigens between the pathogen and the autoantigens targeted by the autoimmune disease.
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.
Chapter 18 Solutions
Becker's World of the Cell (9th Edition)
Ch. 18 - Suppose a triplet on the template strand of a...Ch. 18 - Of these three techniques, which one provides the...Ch. 18 - Compare and contrast bacterial and eukaryotic...Ch. 18 - The autoimmune disease systemic lupus...Ch. 18 - QUANTITATIVE Triplets or Sextuplets? In his Nobel...Ch. 18 - The Genetic Code in a T-Even Phage. A portion of a...Ch. 18 - Frameshift Mutations. Each of the mutants listed...Ch. 18 - Prob. 18.4PSCh. 18 - Locating Promoters. The following table provides...Ch. 18 - Prob. 18.6PS
Ch. 18 - Starting Up. Refer to Figure 18-30, which depicts...Ch. 18 - RNA Processing. The three major classes of RNA...Ch. 18 - Prob. 18.9PSCh. 18 - Antibiotic Inhibitors of Transcription. Rifamycin...Ch. 18 - Prob. 18.11PSCh. 18 - Cloning Conundrum. Using established recombinant...Ch. 18 - Nucleoli. Indicate whether each of the following...
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- You are in the process of developing a monoclonal antibody against an Influenza virus spike protein "H7." You have isolated the B cells producing antibodies against the viral H7 protein and fused those specific B cells with a unique kind of mutant myeloma cells. The myeloma cells can't make any of the three following enzymes; dihydrofolate reductase (DHFR), thymidine kinase (TK), and hypoxanthine-guanosine phosphoribosyl transferase (HGPRT). The mutant unfused myeloma cells are grown in the laboratory in a nucleotide supplemented medium. For selecting the hybridomas, you have used a modified medium HT that does not contain any aminopterin but contains hypoxanthine and thymidine. Which of the following result do you expect to see from your experiment, and what problem you may encounter in the future after the hybridoma selection?arrow_forwardSome viruses have mechanisms to down-regulate MHC class I protein expression on the surface of cells in which the virus is replicating. This immune evasion strategy might prevent effector CD8 cytotoxic T cells from recognizing and killing the virus-infected cells. Would this immune evasion strategy also prevent the initial activation of virus-specific CD8 T cells? Yes, because no viral peptide:MHC class I complexes would form to activate CD8 T cells. No, because dendritic cells would take up infected cells and cross-present viral peptides to activate CD8 T cells. No, because some presentation of MHC class I complexes with viral peptides would occur before the virus could down-regulate all the surface MHC class I protein. Yes, because this immune evasion strategy would also function in dendritic cells, even if the virus doesn’t replicate in dendritic cells. No, because the type I interferon response induced by the virus infection will up-regulate MHC class I expression and override the…arrow_forwardSerum from individuals with high levels of antibody to SARS-CoV2 has been used to treat patients with severe COVID-19. What is ONE way (there are several) that passive immunization with the antibody to the virus could help these patients? HINT: think about what opsonization with antibody could do for the innate immune response.arrow_forward
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