The mammalian immune response includes both innate-response mechanisms and adap- tive-response mechanisms. Which of the following describes a primary advantage provided by the innate immune response? A It produces antibodies with specificity for a large number of antigens. B It enables Killer T cells to destroy pathogens detected in the body. с It enables a rapid defense against foreign antigens detected in the body. D It allows for the destruction of antibodies via phagocytosis.

The mammalian immune response includes both innate-response mechanisms and adap- tive-response mechanisms. Which of the following describes a primary advantage provided by the innate immune response? A It produces antibodies with specificity for a large number of antigens. B It enables Killer T cells to destroy pathogens detected in the body. с It enables a rapid defense against foreign antigens detected in the body. D It allows for the destruction of antibodies via phagocytosis.

Human Physiology: From Cells to Systems (MindTap Course List)

9th Edition

ISBN:9781285866932

Author:Lauralee Sherwood

Publisher:Lauralee Sherwood

Chapter12: Body Defenses

Section: Chapter Questions

Problem 15RE

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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 0
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
Although the complement cascade can be initiated by antibodies bound to the surface of a pathogen, complement activation is generally considered to be an innate immune response. This is because: Two of the three pathways for complement activation are initiated by constitutively produced recognition molecules that directly interact with microbial surfaces. When the complement cascade leads to the formation of a membrane-attack complex, the pathogen is killed. Several of the soluble products generated by complement activation lead promote the inflammatory response. Complement proteins bound to the pathogen promote uptake and destruction by phagocytic cells. The C3 convertase is only produced when complement activation is initiated by antibody binding to a pathogen.
Some 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?
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.
Opsonization of pathogens by both antibodies and complement proteins (C3b) leads to uptake and destruction of the pathogen by phagocytic cells that express both Fc receptors and complement receptors. Which of the following in the figure below is the most efficient form of dual opsonization of the pathogen by antibody and C3b to maximize phagocytosis?
Cytotoxic effector T cells also produce inflammatory cytokines such as IFN-g and TNF-a when their T-cell receptor recognizes peptide:MHC on a target cell. One effect of this cytokine secretion is to enhance the ability of CD8 effector T cells to recognize and kill other infected cells in the nearby vicinity. This enhanced activity is due to: The increased production of perforin and granzymes by CD8 cells The up-regulation of MHC class I protein expression by IFN-g The ability of TNF-a to induce vascular leakage The effect of cytokines on promoting target cell apoptosis The effect of IFN-g to enhance viral replication leading to increased viral antigen presentation
Which of the following is true about innate immune system? Check all that apply. PAMPs recognize pathogen recognition receptors (PRRs) such as TLRs, NLRs and RLRs present on/in host cells TLRs that are expressed on cell surface are mostly recognized by viruses, whereas intracellular TLRs are recognized by bacteria PRRs can induce inflammatory response, opsonization and phagocytosis Pattern associated molecular patterns (PAMPs) are molecules such as CpG DNA, cytosolic dsDNA and RNAs made by the host cell
Which of the following is true about innate immune system? Check all that apply. Rig-I-like receptors have the advantage of recognizing viruses by interacting with their spike proteins TLR signaling includes NF-kB pathways to induce synthesis of proinflammatory cytokines TLR binds to dsDNA or ssRNA to induce interferon gene expression PRR induced secretion of proinflammatory cytokines and chemokines have local and systemic effects PRR induces innate immunity; phagocytosis, inflammation, type I interferon production, and regulate adaptive immunity; DC maturation, costimulatory molecules, type I interferon
Which of the following apply to the specific function of IL-2? OIL-2 promotes vasodilation and vascular permeability OIL-2 promotes rapid mitosis by lymphocytes IL-2 promotes the perforation of the plasma membrane of host cells infected with an intracellular pathogen O None of the statements apply OIL-2 promotes complement-directed lysis of the pathogen OIL-2 promotes fever
The T-cell receptor gene segments are arranged in a similar pattern to immunoglobulin gene segments and are rearranged by the same enzymes. While B cells and T cells differ markedly in their functions during an immune response, the two lymphocyte subsets share the enzymatic machinery and overall scheme for generating antigen receptor diversity. This is because: B cells and T cells recognize the same form of antigen expressed by an infecting pathogen. Animals with B cells developed first, and later evolving species then developed T cells. B cells and T cells both need enormous antigen receptor diversity to provide protection against the diversity of pathogens. Antibody and T-cell receptor gene segments are both flanked by similar recombination signal sequences. B cells and T cells both secrete their antigen receptor proteins after they are activated by antigen-binding.
T cells and B cells have many similarities in how they produce their highly diverse repertoire of antigen receptors, but one important difference between them is that B cell receptors can undergo somatic hypermutation to alter their affinity for antigen. This is known as ‘affinity maturation’, and the result is that the pool of B cells specific for a particular microbe will increase their binding affinity. T cells do not engage in either somatic hypermutation or affinity maturation. Why not? What potential harm could come from allowing T cells to alter the affinity of their TCRs after they have already left the thymus and have become activated in a lymph node or spleen?