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 1R
Summary Introduction
To review:
The working of the cyclosporin drug, which interrupts the development of T cell.
Introduction:
The cyclosporin is a class of immunosuppressant, which is administered to the patients who face organ rejection. The transplanted organ can be rejected by the body due to the cell-mediated immunity, which can be suppressed by the inhibition of the T-cell development. The cyclosporin drug acts by interrupting the development of T cell and suppress the immune system of the patient.
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The innate immune response together with antibodies are generally not effective at clearing infections established by pathogens that replicate inside host cells. The evolution of T cells has provided a means for the immune response to ‘see’ intracellular infections based on the ability of T cells to:
Secrete cytokines that diffuse into the infected tissue
Activate type I interferon production by macrophages and dendritic cells
Activate macrophages to induce inflammation
Recognize pathogen-derived peptides on host MHC surface molecules
Express cytoplasmic sensors for detecting pathogen-derived nucleic acids
What occurs in a cell-mediated immune response? Select all that apply.
Naive B cells bind to antigen on the surface of a bacterium and become activated.
A dendritic cell incorporates digested viral antigen-MHC complexes.
Naive cytotoxic T cells bind to antigen on antigen-presenting dendritic cells and become activated.
Effector cytotoxic T cells circulate through the body and kill any body cells that display the viral antigen-MHC complexes.
Describe how using cells is an important link between the innate immunity and adaptive immunity is formed. Please explain and make some examples.
Chapter 41 Solutions
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- Neutralizing antibodies are effective at preventing infection or toxicity mediated by pathogens or their toxic products. In fact, nearly all vaccines currently in use function by eliciting neutralizing antibodies. One example is the tetanus vaccine, in which neutralizing antibodies are generated against an inactivated form of the tetanus toxin (the tetanus toxoid). The most important feature of a neutralizing antibody is having high affinity for the antigen. being efficient at activating the complement cascade. having a high degree of multivalency, such as being a pentamer or hexamer of immunoglobulin monomers. being present at a high concentration in the circulation. 0 0 0 0arrow_forwardThe 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.arrow_forwardSome strains of the human papilloma virus (HPV) are resistant to interferons. If HPV can inhibit interferon binding to cells, what advantage does this give the virus? Question 2 options: Antiviral proteins will not be synthesized in neighbouring cells. Interferons will be released by non-infected neighbouring cells. Interferons will bind to the virus to neurtralize it. Interferons tell the virus-infected cells to apoptose. The viruses will be warned that a host is coming.arrow_forward
- Although the immune system has two arms, it has been said, “No T cells, no immunity.” How is this so?arrow_forwardThe diagram shows a pathogen (in red) that is present in different cellular compartments of each of the cell types shown. In each case, a specific T cell subset will recognize peptides of that pathogen presented on MHC molecules on the surface of the cell, and will execute its effector function. From the list below, match the appropriate T cell effector response to the cell type and location of the pathogen. CD4 T cell killing of target cell CD8 T cell killing of target cell CD4 T cell activation of target cell’s antibody production CD8 T cell activation of target cell’s antibody production CD4 T cell activation of target cell’s ability to kill intracellular pathogen CD8 T cell activation of target cell’s ability to kill intracellular pathogenarrow_forwardDraw a schematic diagram of a typical IgG molecule and label each of the following parts: H chains, L chains, intrachain disulfide bonds, hinge, Fab, Fc, and all the domains. Indicate which domains are involved in antigen binding.arrow_forward
- Why would a virus that can interfere with a host cell’s production of MHC class I molecules be at an advantage?arrow_forwardDescribe in detail what is meant by a "self- restricted/ self-tolerant" T cell. A diagram is helpful here.arrow_forwardSome primitive organisms, such as invertebrates, have no lymphocytes and thus lack an adaptive immune system, but they have somecomponents of an innate immune system, including phagocytes andcertain protective proteins. What are some general features of innateimmunity that make it very valuable to organisms lacking more specific antibody- and cell-mediated responses? What are some disadvantages to having only an innate immune system?arrow_forward
- Helper T cells are affected by HIV, how come is this receptor key to the immune system? which line of defense are we referring to? How is it connected to the immune system and which line of defense? Hence, based on your prompt, how are cytokines linked to the defense mechanism of HIV virus? Do you know or can you explain the cascade of events dealing with PAMPS, TLRs, interferon? What do they have to do with the second line of defense?arrow_forwardCancer cells evade immune surveillance. What "strategies" can cancer cells use to escape NK cells?arrow_forwardThis week you learned about the role that macrophages, neutrophils, and cytokines play in the innate immune response and looked at how they contribute to the development of inflammation and the inflammatory and the acute phase response. In certain bacterial illnesses, particularly lung infections with Pseudomonas aeruginosa, a physician may not treat the patient with antibiotics (which will kill the microorganisms), but rather give the patient anti-inflammatory medications. Why might a physician choose to inhibit inflammation in the case of an infection? What types of damage might the inflammatory response do to the surrounding tissues, not just the bacteria it was designed to combat?arrow_forward
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