You can tell the difference between an uncommitted progenitor cell and a double negative thymocyte committed to the T cell lineage based upon surface molecules. Which one of the following is not expressed by a double negative thymocyte committed to the T cell lineage? CD1A CD2 CD44 CD127

You can tell the difference between an uncommitted progenitor cell and a double negative thymocyte committed to the T cell lineage based upon surface molecules. Which one of the following is not expressed by a double negative thymocyte committed to the T cell lineage? CD1A CD2 CD44 CD127

Name: You can tell the difference between an uncommitted progenitor cell and
Uploaded: 2024-03-20T06:42:55.000Z
Channel: Bartleby
Description: You can tell the difference between an uncommitted progenitor cell and a double negative thymocyte committed to the T cell lineage based upon surface molecules. Which one of the following is not expressed by a double negative thymocyte committed to t

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 15RE

See similar textbooks

Concept explainers

Mitochondrial Mutations

A mitochondrion is a cellular organelle that serves as the site for cellular respiration and energy production (ATP or Adenosine Triphosphate). It is a double-membrane-bound organelle and is only present in eukaryotic cells.

Topic Video

Question

CD1A

CD2

CD44

CD127

Expert Solution

This question has been solved!

Explore an expertly crafted, step-by-step solution for a thorough understanding of key concepts.

SEE SOLUTION Check out a sample Q&A here

Step by step

Solved in 2 steps

SEE SOLUTION Check out a sample Q&A here

Knowledge Booster

Learn more about

Need a deep-dive on the concept behind this application? Look no further. Learn more about this topic, biology and related others by exploring similar questions and additional content below.

Similar questions

A mouse is infected with staphylococcal bacteria through a laceration in the skin of its paw. Dendritic cells are isolated from the tissue at the site of infection, and are incubated together with naïve staphylococcal-specific CD4 T cells. Seventy-two hours later, the proliferation of the CD4 T cells is measured as a readout for T cell activation. Surprisingly, the T cell response is quite poor compared to the response observed when the same T cells are mixed with a comparable number of dendritic cells isolated from the draining lymph node of the infected mouse. A comparison of the dendritic cells isolated from the two different sites would reveal: Much higher levels of MHC and B7 molecules on the lymph node dendritic cells than those from the infected tissue Much higher expression of all TLRs in the lymph node dendritic cells than those from the infected tissue An increased number of MHC class II molecules bearing bacterial peptides on the surface of dendritic cells from the infected…
The mechanism of cross-presentation by dendritic cells is an essential pathway for generating CD8 T cell responses to some intracellular pathogens. If this pathway did not exist, we would be highly susceptible to: Intracellular pathogens that can survive inside macrophage endocytic vesicles Intracellular pathogens that are able to evade antibody responses Intracellular pathogens that do not infect and replicate in dendritic cells Intracellular pathogens that can spread from cell to cell by inducing cell fusion Intracellular pathogens that infect and replicate in red blood cells
All of the following statements concerning regulatory T cells (Treg) are correct, EXCEPT: The regulatory cytokines produced by regulatory T cells are IL-12 and TGF-B O Thymocytes that recognize self-antigen in the thymus with a certain affinity become natural (central) regulatory T cells O In the periphery T cells that recognize self-antigen in the presence of TGF-B become induced regulatory T cells O A Treg cell can suppress self-reactive lymphocytes that recognize peptides different from that recognized itself provided that the peptides are derived from the same tissue O A Treg cell can suppress self-reactive lymphocytes that recognize peptides different from that recognized by itself provided that the peptides are presented by the same antigen-presenting cell (APC)
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.
Cytotoxic effector T cells also produce inflammatory cytokines such as IFN-g and TNF-a when their T-cell receptor recognizes peptide:MHC on a target cell. One effect of this cytokine secretion is to enhance the ability of CD8 effector T cells to recognize and kill other infected cells in the nearby vicinity. This enhanced activity is due to: The increased production of perforin and granzymes by CD8 cells The up-regulation of MHC class I protein expression by IFN-g The ability of TNF-a to induce vascular leakage The effect of cytokines on promoting target cell apoptosis The effect of IFN-g to enhance viral replication leading to increased viral antigen presentation
During 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.
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
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.
Secondary lymphoid organs (SLOs) are important sites for the initiation of T cell responses via immune priming. Once an antigen-presenting cell (APC) presenting peptide-MHC arrives at a secondary lymphoid organ, it must find a relatively rare T cell clone with a TCR that recognizes its presented peptide-MHC complex. Which of the following features of SLOs increases the likelihood of this APC finding its cognate T cell? Activated APCs are captured by SLO-resident macrophages once they enter via afferent lymphatics, allowing them to be interrogated by T cells Concentrate high densities of T cells within specific zones to enable efficient APC browsing Drain pathogens from infected tissues through the lymphatics, bringing them to secondary lymphoid organs where they can be killed by B cells Contain specialized nutrients that are required for productive TCR signaling following interactions with a cognate APC
CD8 T cells in a culture are analyzed for their ability to produce the cytokine IFN-g, and the numbers of IFN-g-producing CD8 T cells are quantified. As a control, T cells are also stimulated with an irrelevant non-viral peptide (ova) plus dendritic cells. The results are shown in the figure below. Why is the T cell response different between the two lymph node populations?
The figure below shows the characteristic pattern of Ca2+ influx in the red line (wild-type; WT), where TCR stimulation causes a sharp rise in cytoplasmic Ca2+, followed by a slow decline over hours. As shown below, cytoplasmic Ca2+ concentrations do not normally return to baseline for the time course of this experiment. A mutant mouse is identified with a defect in T cell activation in response to TCR stimulation. The calcium response of T cells from the mutant mouse is shown in the blue line. a) Given these data, name three T cell signaling proteins that could be defective in the mutant T cells. b) Name three T cell signaling proteins that could not be responsible for this defect, even if mutated.
The 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 mice