Brock Biology of Microorganisms (15th Edition)
15th Edition
ISBN: 9780134261928
Author: Michael T. Madigan, Kelly S. Bender, Daniel H. Buckley, W. Matthew Sattley, David A. Stahl
Publisher: PEARSON
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Chapter 27.10, Problem 1MQ
Describe the binding site for superantigens on T cells and APCs. How does this relate to the activation of a much larger population of T cells than normal upon exposure to superantigens?
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Which proteins involved in the activation of T cells have the capacity for transduction without the need to be activated by a family of kinases?
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.
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. 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?
Chapter 27 Solutions
Brock Biology of Microorganisms (15th Edition)
Ch. 27.1 - Prob. 1MQCh. 27.1 - Prob. 2MQCh. 27.1 - Distinguish between clonal deletion and clonal...Ch. 27.1 - QWhy is it necessary that all three defining...Ch. 27.2 - Identify the intrinsic and extrinsic properties of...Ch. 27.2 - Describe an epitope recognized by an antibody, and...Ch. 27.2 - Give an example for each: natural and artificial...Ch. 27.2 - QWhat properties are required for a vaccine to...Ch. 27.3 - Summarize antibody production starting with...Ch. 27.3 - Differentiate among antibody classes using...
Ch. 27.3 - Prob. 3MQCh. 27.3 - QDescribe the structural and functional...Ch. 27.4 - Draw a complete Ig molecule and identify...Ch. 27.4 - Describe antigen binding to the CDR1, 2, and 3...Ch. 27.4 - Describe the recombination events that produce a...Ch. 27.4 - QWhich Ig chains are used to construct a complete...Ch. 27.5 - Identify the cells that display MHC class I and...Ch. 27.5 - Compare the MHC I and MHC II protein structures...Ch. 27.5 - Define the sequence of events for processing and...Ch. 27.5 - QDescribe the basic structure of class I and class...Ch. 27.6 - Define polymorphism and polygeny as they apply to...Ch. 27.6 - How does a single MHC protein present many...Ch. 27.6 - QPolymorphism implies that each different MHC...Ch. 27.7 - Prob. 1MQCh. 27.7 - Identify diversity-generating mechanisms unique to...Ch. 27.7 - Describe and compare the structural features of Ig...Ch. 27.7 - QWhat diversity-generating mechanisms function to...Ch. 27.8 - Describe the mechanism used by Tc cells to...Ch. 27.8 - Describe the effector system (the cell-killing...Ch. 27.8 - Compare and contrast the roles and activities of...Ch. 27.8 - QWhat mechanism do Tc cells use to identify and...Ch. 27.9 - Discriminate between immediate hypersensitivity...Ch. 27.9 - Provide examples and mechanisms for an...Ch. 27.9 - QHow do immediate and delayed-type...Ch. 27.10 - Describe the binding site for superantigens on T...Ch. 27.10 - Compare and contrast the immunodeficiency observed...Ch. 27.10 - Prob. 3MQCh. 27.10 - Prob. 1CRCh. 27 - Antibodies of the IgA class are probably more...Ch. 27 - Prob. 2AQCh. 27 - Polymorphism implies that each different MHC...Ch. 27 - What problems would arise if a person had a...
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- To avoid the potential for activating self-reactive T cells that might cause autoimmunity, naive T cell activation has stringent requirements for co-stimulatory signals in addition to the engagement of T-cell receptors with peptide: MHC complexes. Yet this requirement is abandoned once T cells have differentiated into effector cells. Name two effector T cell functions that would fail if effector T cells also required T-cell receptor signals plus co-stimulatory signals through CD28 to elicit their effector responses.arrow_forwardDuring the early developmental stages of α:β T cells in the thymus, there are two key checkpoints that must be satisfied to permit the progression of T-cell development. Explain what occurs at each checkpoint.arrow_forwardT cells can differentiate into 5 different subsets of helper T cells. Answer the following questions for TH1 cells: A) In general, list three unique factors that differentiate the TH1 subset from the other subsets. B) For each of those factors identified in A, provide one specific example that applies to TH1 cells. C) What type of pathogens are targeted by the TH1 cells?arrow_forward
- Influenza virus causes serious disease and death, and is responsible for one of the largest pandemics in recorded history. However, the process by which antigens are made and processed are not unique to that virus. Answer the following questions to trace how infected cells will become recognizable by the TCR of a compatible T-cell. A) Where are the viral proteins made? B) Describe the process by which viral proteins are broken down into peptides. Be sure to discuss any unique molecules or organelles that participate in the process. C) Which MHC molecule presents these peptides? D) Now that you have made peptides from the viral antigen, how do they get to and bind to the MHC molecule? Describe the process. What unique molecules are involved in this process? E) What is the final destination for these molecules/epitopes, and how do they reach that destination?arrow_forwardWhat is a T-cell receptor and how is it involved in T-cell activation?arrow_forwardIgM antibodies are much more efficient than IgG at activating the complement cascade. However, under certain circumstances, IgG antibodies will activate the complement pathway. One example of a situation in which IgG binding to its antigen will not trigger the complement cascade is when the IgG antibodies are neutralizing a bacterial toxin protein by blocking the receptor-attachment site on the toxin. the IgG antibodies are binding self-antigens, such as chromatin released from dead cells. the IgG antibodies bind to a bacterial surface by recognizing a repetitive polysaccharide component of the bacterial capsule. the IgG antibodies bind to a viral capsid protein that is present in more than 100 copies on the viral particle surface.arrow_forward
- TCR and CD28 signaling together leads to maximal production of IL-2 by the activated T cell. Experiments investigating the mechanism underlying the CD28 co-stimulation-mediated increase in IL-2 production show that T cells stimulated through the TCR plus CD28 have increased levels of IL-2 mRNA compared to cells stimulated through the TCR alone. One important component contributing to increased IL-2 mRNA levels is increased mRNA stability after transcription and splicing. increased glucose metabolism due to increased production of glycolytic enzymes. increased protein synthesis due to increased production of ribosomes. enhanced mRNA transport from the nucleus to the cytoplasm. 0 0 0 0arrow_forwardWhat are the similarities and divergences between Immunoglobulin and T-Cell Receptor (TCR) rearrangement? What are the genes and key enzymes involved in this process?arrow_forward1:Describe the various stages of T cells and the events that occur during each of these stages during T cell development. What stages of T cell development would be affected in mice with the following genetic mutations? Justify your answer. a) Mice that do not express MHC Class I molecule. b) Mice that do not express Rag1 c) Mice that do not express the pre-T-alpha chain 2:Transgenic mice that have constitutive expression of Rag1/2 are being used in an experiment to study pre-BCR signaling. Based on your knowledge of early B cell development, speculate on what might be the fate of BCR rearrangement and how will this affect further development of B cells in the bone marrow? please answer in full detail I want long well explained answers.arrow_forward
- Which of the following is part of the T-cell clonal deletion process? a) T-cells are eliminated if they bind to B-cells b) Lymphocytes that bind to MHC undergo apoptosis c) T-cells that bind to the same antigen as B-cells are eliminated d) Lymphocytes that react to autoantigens undearrow_forwardThe current view in the field of immunology is that dendritic cells are the primary antigen-presenting cells for stimulating naive T cells. One piece of evidence supporting this conclusion is the observation that IRF8-deficient individuals, which retain their tissue-resident macrophages, are susceptible to a range of severe opportunistic infections caused by intracellular bacteria, viruses, and fungi. Explain the reasoning behind this argument.arrow_forwardCyclosporin A and rapamycin are each used as T cell immunosuppressants. They share the property of binding to immunophilin molecules in T cells as the initial step in their mechanisms of action. However, in the case of cyclosporin A, the drug:immunophilin complex binds to and inhibits the protein phosphatase calcineurin, whereas the rapamycin:immunophilin complex binds to and inhibitors mTOR. As a consequence, Cyclosporin A, but not rapamycin, blocks cytokine production by T cells. Both cyclosporin A and rapamycin block cytokine production by T cells. Rapamycin, but not cyclosporin A, blocks T cell proliferation. Neither rapamycin nor cyclosporin A block T cell proliferation. Both cyclosporin A and rapamycin inhibit co-stimulatory signaling through CD28 on T cells.arrow_forward
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