Brock Biology of Microorganisms - MasteringBiology With eText - Access
15th Edition
ISBN: 9780134602288
Author: MADIGAN
Publisher: PEARSON
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Chapter 26.10, Problem 1CR
Summary Introduction
Natural killer cells which are also called NK cells are cytotoxic lymphocytes that are different from B cells (B lymphocytes) and T cells (T lymphocytes). These natural killer cells degrade the cells which are infected by intracellular pathogens or cancer cells. A T-cytotoxic cell is T lymphocyte which kills cancerous cells or cells infected with viruses.
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B cells express a complement receptor that binds to C3b cleavage products, such as iC3b and C3dg. When a B cell with an antigen receptor that specifically recognizes that pathogen also has its complement receptor stimulated because the pathogen is opsonized with these C3 fragments, B cell activation is greatly enhanced. Due to this mechanism, B cells can be activated by much lower concentrations of antigen (in this case, the pathogen) than if the antigen is devoid of complement components. This mechanism functions to:
Ensure that pathogens are readily detected by the adaptive immune system before they replicate to high levels in the host
Prevent B cells from being activated in response to antigens that are not pathogens
Allow B cells to phagocytose the pathogen and help destroy it
Induce increased rounds of B cell replication to make more pathogen-specific B cells
Allow the B cell to block pathogen replication by interfering with multiple pathogen surface functions
Why is the concentration of this ligand for the NK-cell receptor CD94:NKG2A. on the target cell an effective measure of the presence or absence of classical MHC class I molecules?
Why is this ligand for the NK-cell receptor CD94:NKG2A. considered a broad mechanism for the NK-cell detection of unhealthy cells that is relatively insensitive to MHC class I polymorphisms?
Chapter 26 Solutions
Brock Biology of Microorganisms - MasteringBiology With eText - Access
Ch. 26.1 - What major class of immune cells mediates an...Ch. 26.1 - Prob. 2MQCh. 26.1 - Compare and contrast the major features of innate...Ch. 26.2 - Describe host tissue specificity for pathogens.Ch. 26.2 - Identify physical and chemical barriers to...Ch. 26.2 - What other factors may control the outcome of an...Ch. 26.2 - Identify at least four mechanisms by which a...Ch. 26.3 - Describe the circulation of a leukocyte from the...Ch. 26.3 - What soluble molecules determine whether a...Ch. 26.3 - Cells involved in innate and adaptive immunity...
Ch. 26.4 - How does the development of B, T, and NK cells...Ch. 26.4 - Distinguish between the primary lymphoid organs...Ch. 26.4 - Leukocytes are differentiated white blood cells...Ch. 26.5 - Although technically not part of the immune...Ch. 26.5 - Describe the mechanisms by which circulating...Ch. 26.5 - Pathogens may colonize host tissues when...Ch. 26.6 - Identify a PAMP shared by a group of...Ch. 26.6 - Outline the general features of a signal...Ch. 26.6 - Innate recognition of common pathogens occurs...Ch. 26.7 - Identify the mechanism used by phagocytes to...Ch. 26.7 - Describe several reasons why phagocytes are not...Ch. 26.7 - Phagocytosis is the engulfing of infectious...Ch. 26.8 - Prob. 1MQCh. 26.8 - Identify the major symptoms of localized...Ch. 26.8 - Fever and inflammation, characterized by pain,...Ch. 26.9 - In what ways does the classical pathway of...Ch. 26.9 - What is opsonization, and how does opsonization...Ch. 26.9 - Why are the mannose-binding lectin and alternative...Ch. 26.9 - The complement system is composed of soluble...Ch. 26.10 - Prob. 1MQCh. 26.10 - Prob. 2MQCh. 26.10 - Prob. 1CRCh. 26 - Prob. 1AQCh. 26 - Describe the potential problems that would arise...Ch. 26 - Prob. 3AQCh. 26 - Prob. 4AQ
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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.arrow_forwardIngestion of complement-tagged pathogens by phagocytes is mediated by receptors for the bound complement proteins. Even when the complement cascade fails to proceed beyond generating the C3 convertase, complement activation is effective at inducing pathogen uptake and destruction. This process of immune protection is mediated by: Activation of complement inhibitory receptors on phagocytes that promote pathogen uptake Activation of soluble proteases in the serum that disrupt pathogen membranes Engagement of complement receptors on phagocytes by C3b and its cleavage products which promotes phagocytosis Engagement of complement receptors on B cells that promotes antibody production Stimulation of antimicrobial peptide secretion by phagocytesarrow_forwardOpsonization 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?arrow_forward
- 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…arrow_forwardMany cells in the human body have proteins on the surface that are able to interact with the receptors of helper T cells. Explain the mechanisms and why it is that such an interaction or signal does not usually result in an autoimmune reaction?arrow_forwardWhat is the relationship and differences between receptor-mediated endocytosis and TLR in relation to innate immunity?arrow_forward
- Inflammation is the hallmark of an activated immune response. Explain how inflammation is triggered by both innate and adaptive immune mechanisms. Are the inflammatory cells the same for both methods of activation? Why does inflammation subside as an infection is controlled?arrow_forwardWhat is the activation signal for NK cells? How doesthis differ from the activity of T-cytotoxic lymphocytes?arrow_forwardGenerally speaking, what kinds of cells express MHC I, MHC II, or both? What is presented on MHC I and II, and what kind of T cell recognizes each one? What response occurs when a T cell recognizes what is being presented on MHC I? What happens if it recognizes MHC II? Give an example of each type of recognition.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_forwardDuring the chemotaxis phase of the inflammatory response,a. C-reactive protein is secreted by damaged parenchymal cells in the tissue, which attracts neutrophils, which secrete leukotrienes and prostaglandins to attract macrophages; a purulent exudate is formed.b. Band cells respond to hyperthermia by producing TNF-α and interleukins, which then cause a left shift that results in the accumulation of neutrophils within the tissue.c. Damaged parenchymal cells release prostaglandins and leukotrienes to attract macrophages, causing a left shift and the formation of a purulent exudate.d. Cytokines, such as TNF-α, are released by damaged parenchymal cells, while leukotrienes and prostaglandins produced by neutrophils cause smooth muscle constriction and the further accumulation of leukocytes.arrow_forwardIn regard to antigen presentation, MHC class I molecules usually present peptides derived from _____, whereas MHC class II molecules usually present peptides derived from _____. a. intracellular cytosolic sources; vesicular system b. phagolysosome; proteasomes c. MIIC; self proteins d. CLIP; HLA-DM e. endocytic vesicles; endoplasmic reticulum.arrow_forward
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