Human Anatomy & Physiology (11th Edition)
11th Edition
ISBN: 9780134580999
Author: Elaine N. Marieb, Katja N. Hoehn
Publisher: PEARSON
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In B cells, what mechanism ensures that only rearranged V genes are transcribed?
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- What is the function of interleukin-7 in lymphocyte formation? View Available Hint(s) Hint 1. Development of Lymphocyte Types opened hint The different lymphocyte types are all derived from lymphatic stem cells. Their ultimate fate depends upon the location where they mature and the signals that they receive. What is the function of interleukin-7 in lymphocyte formation? It supports the differentiation of lymphoid stem cells into NK, B, and T cells. It supports the differentiation of pluripotential stem cells into lymphoid stem cells. It supports the differentiation of pluripotential stem cells into NK, B, and T cells. It supports the differentiation of lymphoid stem cells into NK cells and B cells.arrow_forwardWhat is apoptosis and how is it utilized as a quality control mechanism in cellular and humoral immune responses?arrow_forwardWhich statement best summarizes the two types of cells that B cells differentiate to form? a.) B cells can become plasma cells, which formm antibodies, or memory cells, which help mount an immune response quickly if a pathogen infects the host again. b.) B cells can become plasma cells, which coordinate cell-mediated immunity, or memory cells, which are responsible for endocrine signaling. c.) B cells can become memory cellsm which coordinate cell-mediated immunity, or plasma cells, which are responsible for endocrine signaling/ d.) B cells can become memory cells, which form antibodies, or plasma cells, which help mount an immune response quickly if a pathogen infects the host again.arrow_forward
- The B-cell co-receptor, composed of CD19/CD21/CD81, is a receptor that binds to complement fragments such as C3dg. When an antigen bound by the BCR on a B cell has also been tagged with C3dg, the B-cell co-receptor is stimulated together with the BCR. Signaling through the co-receptor inhibits BCR signaling by leading to PIP3 dephosphorylation. inhibits BCR signaling by leading to ITAM dephosphorylation. enhances BCR signaling by recruiting and activating PI 3-kinase. enhances BCR signaling by bringing the Src kinase together with Ig-a and Ig-ß.arrow_forwardWiskott–Aldrich syndrome is an immunodeficiency disease due to mutations in the gene encoding WASp. Individuals with this disease make poor antibody responses to protein antigens, due to impaired T cell help for B cells. WASp-deficient T cells are likely impaired in providing adequate help to B cells due to: A. Defects in up-regulating expression of genes encoding cytokines required by B cells B. Defects in up-regulating metabolic pathways for T cell macromolecular synthesis C. Defects in up-regulating expression of genes needed for T cell survival D. Defects in cytoskeletal reorganization needed for directed T cell cytokine secretion E. Defects in up-regulating T cell integrin adhesion for stable interactions with B cellsarrow_forwardIf a centrocyte does not interact with antigen and engage CD40 shortly after its derivation, then Select one: a. it recommences somatic hypermutation b. it undergoes apoptosis C. it moves back into the dark zone of the germinal center and switches its isotype d. its surface immunogloblulin levels decrease and proliferation recommences.arrow_forward
- why is clonal deletion so important? how does it differ from clonal selection?arrow_forwardWhich of the following characteristics is true of large Pre-B cells? Select one: a. They do not express CD19 at the cell surface. b. Rearrangement of light-chain genes commences. c. Nonproductive rearrangement of both heavy-chain loci has already occurred. d. Allelic exclusion of the immunoglobulin light-chain loci has already occurred. u is assembled with VpreB25. e.arrow_forwardThe TNF family of cytokines and their receptors are critical for the development of secondary lymphoid organs, such as the lymph nodes and Peyer’s patches. As a consequence, knockout mice lacking expression of LT-b fail to develop most of these structures. Reconstitution of irradiated LT-b-deficient mice with bone marrow stem cells from wild-type mice (e.g., LT-b-sufficient) would: Restore all missing lymphoid structures in the recipient mice Restore the missing lymphoid structures but not the missing follicular dendritic cells in the recipient mice Restore the missing follicular dendritic cells but not the missing lymphoid structures in the recipient mice Have no effect on any lymphoid structures in the recipient mice Only restore the proper organization of B cell follicles in the recipient micearrow_forward
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