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.

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.

Human Heredity: Principles and Issues (MindTap Course List)

11th Edition

ISBN:9781305251052

Author:Michael Cummings

Publisher:Michael Cummings

Chapter17: Genes And The Immune System

Section: Chapter Questions

Problem 13QP: The Adaptive Immune Response Is a Specific Defense Against Infection In cystic fibrosis gene...

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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.
Defects in antigen receptor gene rearrangement can result in SCID (severe combined immunodeficiency). Infants with RS-SCID (radiation-sensitive SCID) generally require treatment by bone marrow transplantation from a healthy donor. In this treatment, hematopoietic stem cells from the donor will give rise to normal B and T lymphocytes, thereby restoring normal immune function. However, the bone marrow transplantation treatment does not alter the high incidence of cancer in these patients. Why not?
Mice and humans with inactivating mutations in the gene encoding activation-induced cytidine deaminase (AID) have an immunodeficiency disease known as 'hyper IgM type 2'. Since AID is the enzyme that catalyzes the conversion of cytosines in the DNA to uracils, thereby initiating the process of somatic hypermutation, why do individuals with this deficiency only produce IgM antibodies?
Entanercept is a pharmaceutical that is composed of a recombinant receptor for human tumor necrosis factor, fused to the Fc portion of the immunoglobulin IgG. How does it work?
Why Somatic Hyper Mutation takes place in B-Cells only and not in T-Cells?
Researchers can make monoclonal antibodies by immunizing a mouse with a molecule (or with a microorganism). The resulting antibody-mediated response produces a set of antibodies that recognize different parts of the molecule. The mouse's B cells are then harvested from its spleen and fused with cancerous B cells from a myeloma cell line. The resulting hybrid myeloma ("hybridoma") cells are cloned: Individual cells are grown in tissue culture as separate cell lines. Each cell line produces and secretes antibodies that recognize one part of the immunizing molecule. These antibodies are called monoclonal antibodies, and they can be purified and used for research or other purposes. Monoclonal antibodies are effective for passive immunization, but only in the immediate term. Antibodies produced by one's own immune system can last up to about six months in the bloodstream, but monoclonals delivered in passive immunization often last for less than a week. Why the difference?
For many years it was a complete mystery howcytotoxic T cells could see a viral protein that seemed to bepresent only in the nucleus of the virus-infected cell. Theanswer was revealed in a classic paper that took advan-tage of a clone of T cells whose T cell receptor was directedagainst an antigen assoicated with the nuclear protein ofthe 1968 strain of influenza virus. The authors of the paperfound that when they incubated high concentrations ofcertain peptides derived from the viral nuclear protein, thecells became sensitive to lysis by subsequent incubationwith the cytotoxic T cells. Using various peptides from the1968 strain and the 1934 strain (with which the cytotoxic Tcells did not react), the authors defined the particular pep-tide responsible for the T cell response (Figure Q24–1).A. Which part of the viral protein gives rise to thepeptide that is recognized by the clone of cytotoxic T cells? Why do not all viral peptides sensitize the target cells forlysis by the cytotoxic T…
Chimeric mice are generated where approximately 50% of the cells in the animal are genetically MHC class I-deficient. The other 50% are deficient for the herpes virus receptor, HVEM, but do express MHC class I molecules. When these mice are infected with herpesvirus by intraperitoneal injection, a robust virus-specific CD8 T cell response is detected at day 7 post-infection in the spleens of the infected mice. Which cells are presenting herpesvirus antigens to prime the CD8 T cell response, and how did they acquire the viral antigens?
A mutant B cell line is examined by confocal microscopy after incubation with a microbial pathogen recognized by the BCR on these B cells. The B cells have been stained with antibodies to visualize the localization of polymerized actin and microtubules. As a control, wild-type B cells are examined. The results are shown in the figure below, with the numbers indicating the proportion of cells examined that show each pattern of staining. To identify the specific signaling defect in these mutant B cells, a reasonable biochemical assay would be to: Determine if BCR stimulation of mutant B cells produces enhanced binding of the B cell to the microbe Determine whether the mutant B cells have reduced levels of the enzyme Protein kinase C-q Determine whether the mutant B cells are overexpressing the enzyme Vav Determine whether BCR stimulation of mutant B cells promotes exchange of GDP for GTP on cdc42 Determine whether BCR stimulation of mutant B cells produces increased levels of DAG
The Adaptive Immune Response Is a Specific Defense Against Infection In cystic fibrosis gene therapy, scientists propose the use of viral vectors to deliver normal genes to cells in the lungs. What immunological risks are involved in this procedure?
(a) Identify both the cellular component and the location of the component that is responsible for producing the luciferase protein from mRNAs transcribed in the plasmid-containing T lymphocytes. Explain what dictates to the lymphocytes the correct order in which amino acids should be linked to form the luciferase protein.
B cell receptor diversity is behind our ability to fight new infections. However, epitope-specific B Cell memory is critical for the secondary immune response protecting against new infections. You are ready to integrate concepts. In this question, you will combine B Cell receptor diversity and cloning! Please answer each question in less than 150 characters (including spaces). 1.Can a mature B Cell produce an epitope-specific antibody first and then switch to make an antibody against a different epitope? Explain. 2.Please describe what is transferred into an egg during cloning by somatic nuclear cell transfer. 3.How many B Cell receptors/antibodies could be generated in a mouse cloned by somatic nuclear cell transfer from a mature B Cell (after recombination)?