Life: The Science of Biology
11th Edition
ISBN: 9781319010164
Author: David E. Sadava, David M. Hillis, H. Craig Heller, Sally D. Hacker
Publisher: W. H. Freeman
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Chapter 41.5, Problem 2R
Summary Introduction
To review:
The response, generated by the immune system when a cell gets infected by a virus and the roles played by major histocompatibility complex (MHC) and the T-cell receptors in this type of response.
Introduction:
The viral infection results in the generation of the innate immune responses in the body of the individual. The adaptive immune responses have two components, the humoral and the cell-mediated immune responses. The humoral response kills the virus from the blood and the cell-mediated immunity kill the infected T-cell.
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The classical complement pathway is initiated by C1q binding to the surface of a pathogen. In some cases, C1q can directly bind the pathogen, for instance by recognizing proteins of bacterial cell walls, but in most cases C1q binds to IgM antibodies that are bound to the pathogen surface. How does this IgM-binding feature of C1q contribute to rapid, innate immune responses rather than to slow, adaptive responses?
C1q induces B lymphocytes to begin secreting antibody within hours of pathogen exposure.
Natural antibody that binds to many microbial pathogens is produced prior to pathogen exposure.
C1q binds to C-reactive protein which then binds to IgM on the pathogen surface.
C1q directly induces inflammation, recruiting phagocytes and antibodies from the blood into the infected tissue.
C1q binds to dendritic cells in the infected tissue, inducing them to secrete inflammatory cytokines.
Some 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…
In the cell-mediated immune response, there are three types of T cells produced. What are they, and what is the function of each?
Chapter 41 Solutions
Life: The Science of Biology
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- Where is the CD4 receptor? What is it’s role in the immune response? (provide details – innate vs acquired) Why is someone lacking the CD4 receptor immune to HIV infection?arrow_forwardIt's the first day of university exams and Sarah has woken up with a sore throat, headache, muscle aches and a low grade fever. Her GP diagnoses her with a viral infection and tells her to go home, rest and drink plenty of fluids.Question 1A:Name one of the most likely innate immune system receptors to initially detect this infection and where in host cells this receptor is located? Question 1B: Which cytokine primarily drives the innate anti-viral host response? Question 1C: Describe the antiviral signaling events that take place inside an infected cell in response to this cytokine. Question 1D: Provide a biological explanation for why Sarah was more likely to suffer a viral infection during her periodarrow_forwardWhat are the roles of the following cytokines in defense against infections: 1) TNF 2) IL-12 3) Type I Interferonarrow_forward
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