In the antibody-mediated immune response, the binding of some antigen-presenting cells to helper T cells initiates a signal transduction pathway that transforms the B cells into plasma cells, which will synthesize and secrete large quantities of antibodies-a specialized subset of proteins responsible for attaching to the antigen on the outer surface of pathogens. Which of the following describes the most relevant intracellular change to B cells as they are transformed into plasma cells? A B с D an increase in the surface area of the rough endoplasmic reticulum in order to allow the binding of a large number of ribosomes for antibody synthesis a breakdown of some membrane-bound proteins to allow synthesized antibodies to more readily diffuse across the membrane of the plasma cell an increase in the number of lysosomes in order to facilitate the storage of synthesized antibodies ahead of their transport out of the cell an increase in the volume of the mitochondria in order to increase the rate of ATP pro- duction that will power antibody synthesis

In the antibody-mediated immune response, the binding of some antigen-presenting cells to helper T cells initiates a signal transduction pathway that transforms the B cells into plasma cells, which will synthesize and secrete large quantities of antibodies-a specialized subset of proteins responsible for attaching to the antigen on the outer surface of pathogens. Which of the following describes the most relevant intracellular change to B cells as they are transformed into plasma cells? A B с D an increase in the surface area of the rough endoplasmic reticulum in order to allow the binding of a large number of ribosomes for antibody synthesis a breakdown of some membrane-bound proteins to allow synthesized antibodies to more readily diffuse across the membrane of the plasma cell an increase in the number of lysosomes in order to facilitate the storage of synthesized antibodies ahead of their transport out of the cell an increase in the volume of the mitochondria in order to increase the rate of ATP pro- duction that will power antibody synthesis

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 1SQE

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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
The entry of naive T cells from the blood into lymph nodes and mucosal lymphoid tissues occurs by a process that involves similar steps and similar adhesion molecules to the process by which leukocytes are recruited into sites of inflammation. Yet naive T cells do not enter tissues at sites of inflammation, but rather, home to lymphoid tissues. Which class of adhesion molecules direct the specific homing of naive T cells to lymphoid tissues?
The white blood cells known as T lymphocytes respond to antigens thatbind specifi cally to the T cell receptor, which consists of an antigen-binding αβ transmembrane protein as well as a set of transmembrane signaltransducing proteins known as CD3 that are targets of NRTKs. Thecytoplasmic domains of the CD3 proteins are positively charged and, in the absence of antigen, interact with the intracellular surface of the plasma membrane in such a way that buries several of their Tyr residues in the lipidbilayer. Antigen binding to the T cell receptor leads to a localized infl ux ofCa2+ ions. (a) Explain how a high concentration of Ca2+ could promote phosphorylation and activation of the CD3 proteins. (b) Would this henomenon make the T lymphocyte more or less responsive to the antigen?
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?
Inhibitory receptors on lymphocytes down-regulate immune responses by recruiting protein or lipid phosphatases.BCR signaling on B cells is initiated by antigen binding, leading to mTOR activation. This occurs, for instance, when the antigen is a live microbe that binds to the BCR on the B cells. Which one of the forms of antigen shown below the graph would correctly account for the data shown in the figure?
Explain why each choice (a-d) is correct or incorrect. In order for an antigen to activate or sensitize a T helper cell, the antigen must be a. coated with antibodies b. displayed on the surface of an APC along with MHC antigens c. displayed on the surface of another T cell with IgD antibodies d. partly digested by a natural killer cell
B lymphocytes, the precursors of plasma cells, are triggered to proliferate by the binding of multivalent antigens to receptors on their surfaces. The cellsurface receptors are transmembrane immunoglobulins. Univalent antigens, in contrast, do not activate B cells. (a) What do these findings reveal about the mechanism of B-cell activation? (b) How might antibodies be used to activate B cells?
Explain the mechanism by which (A) macrophages and NK cells, and (B) macrophages and effector T cells become mutually activated in the course of an innate and adaptive immune response, respectively. (C) Which gene defects would impair these mutual activation processes?
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?
During 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.
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.
When T cells are activated by recognizing peptide:MHC complexes on dendritic cells in the lymph node, they up-regulate the receptor CD69. For T cells expressing a given T-cell receptor, the initial strength of the T-cell receptor signal can be modulated by varying the number of peptide:MHC complexes on the dendritic cells, or by varying the affinity with which the T cell-receptor binds to the peptide:MHC complexes. As a result, T cells stimulated with stronger T-cell receptor signals will maintain high expression of CD69 for one or two days longer that if those same T cells were stimulated with weaker T-cell receptor signals. Therefore, T cells stimulated with weaker T-cell receptor signals are likely to: Die by apoptosis Undergo more rounds of proliferation that T cells stimulated with stronger T-cell receptor signals Migrate to the B-cell zones of the lymph node Have reduced effector functions, such as cytokine production Egress from the lymph node 1–2 days earlier than T cells…