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 acti

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 acti

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?
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…
A primary difference between how B cells recognize antigen and how T cells recognize antigen is that a. T-cell receptors can bind antigen only after secretion of the T-cell receptor from the surface of the T cell b. antibodies can bind only to denatured proteins c. T-cell receptors can bind to carbohydrate groups or clusters of amino acids d. B cells recognize degraded proteins bound to major histocompatibility molecules e. T cells recognize degraded proteins bound to major histocompatibility molecules.
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…
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?
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.
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.
The genetic content of each somatic cell in an organism is the same, but not all genes are expressed in every cell. Why can't cells express all the genes they have?
In a mixed lymphocyte reaction, T cells from individual A make a robust response to antigen-presenting-cells from individual B, as long as the two individuals express different alleles of MHC molecules. Estimates indicate that up to 10% of the T cells from individual A may contribute to this response. If one performed this assay using responder T cells from a child and antigen-presenting cells from one parent, the result would be: A massive proliferative response made by the antigen-presenting cells of the parent A very weak response by the child’s T cells, involving only 0.1% of their T cells The complete absence of any proliferative response by the child’s T cells A robust cytolytic response that kills all of the parent’s antigen-presenting cells A robust response by the child’s T cells
To study the immune responses that provide protection against tumor growth in mice, some investigations have used the EL4 mouse thymoma line. This tumor cell line was derived from a C57BL/6 mouse, and represents a type of T cell lymphoma. When transplanted into Rag-deficient mice, the mice rapidly succumb to the tumor. This is also the case when the mice receive wild-type C57BL/6 T cells the day before tumor cell injection. However, Rag-deficient mice were protected when the transferred T cells came from mice that lacked expression of one cytokine receptor, as shown in the fugure below. Name one likely candidate for the cytokine receptor that is knocked out in the T cells that are able to protect the mice.
B cells are specialized blood cells that secrete antibodies. Normally, human blood has millions of differenttypes of B cells making millions of different kinds ofantibody molecules. This variety occurs because, as described in the Fast Forward Box in Chapter 13 entitledProgrammed DNA Rearrangements and the ImmuneSystem, antibody genes undergo rearrangements in theprecursors of B cells. Individual B cell precursorsrearrange their antibody genes in different ways.In the blood of patients with cancers called B celllymphomas, almost all of the antibody molecules areall of one type, but this single type of antibody isdifferent in different lymphoma patients.a. Based on this information, provide a brief description of the genesis of B cell lymphomas, focusingon the cells that are overproliferating.