Toll-like receptors represent an ancient pathogen-recognition system. The first pattern recognition receptor (PRR) important in innate immune responses was discovered in the fruit fly Drosophila melanogaster. Stimulation of this receptor, called Toll, induces: The synthesis of prostaglandins and leukotrienes The inflammatory response in Drosophila hemolymph vessels The production of antimicrobial peptides The recruitment of phagocytic cells to the site of infection The activation of Drosophila complement

Toll-like receptors represent an ancient pathogen-recognition system. The first pattern recognition receptor (PRR) important in innate immune responses was discovered in the fruit fly Drosophila melanogaster. Stimulation of this receptor, called Toll, induces: The synthesis of prostaglandins and leukotrienes The inflammatory response in Drosophila hemolymph vessels The production of antimicrobial peptides The recruitment of phagocytic cells to the site of infection The activation of Drosophila complement

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 6RE

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The Gram-negative bacterium Yersinia pestis, thecausative agent of the plague, is extremely virulent. Uponinfection, Y. pestis injects a set of effector proteins intomacrophages that suppresses their phagocytic behaviorand also interferes with their innate immune responses.One of the effector proteins, YopJ, acetylates serines andthreonines on various MAP kinases, including the MAPkinase kinase kinase TAK1, which controls a key signalingstep in the innate immune response pathway. To deter-mine how YopJ interferes with TAK1, you transfect humancells with active YopJ (YopJWT) or inactive YopJ (YopJCA)and with FLAG-tagged active TAK1 (TAK1WT) or inactiveTAK1 (TAK1K63W), and assay for total TAK1 and for phos-phorylated TAK1, using antibodies against the FLAG tag oragainst phosphorylated TAK1 (Figure Q23–1). How doesYopJ block the TAK1 signaling pathway? How do you sup-pose the serine/threonine acetylase activity of YopJ mightinterfere with TAK1 activation?
Based on these data, where would you MOST likely find toll-like receptor-XX (TLR-XX) among the following options? Justify WHY you selected that option.Your justification must be based on the data that are presented here, not the type of bacteria. A. On the cell surface B. In the endosome/ lysosome C. In the nucleus D. In the mitochondria E. In the endoplasmic reticulum
Mammalian Toll-like receptors are activated by many different pathogen-associated molecular patterns. As a family, TLRs can recognize PAMPs associated with a broad array of different pathogens, including bacteria, viruses, and fungi. Patients with a specific susceptibility to herpesvirus infections have a defect in their ability to respond to viral nucleic acids using TLR-3, TLR-7, or TLR-9, even though these proteins are expressed in the patients’ cells. Analysis of the TLRs in macrophages and dendritic cells from these patients would likely show which of the arrangements in Figure below?
TLR-4 recognizes bacterial lipopolysaccharide in association with the host accessory proteins MD-2 and CD14. Stimulation of the nucleic acid sensing TLRs that reside in endosomal membranes induces the production of a different cytokine response than is produced by stimulation of the plasma membrane TLRs. In part, this distinction is based on the different adapter proteins used by the nucleic acid sensing TLRs, leading to the activation of IRF factors. The cytokine response following stimulation of nucleic acid-sensing TLRs is characterized by production of: The antiviral cytokine, type I interferon TNF-a, which induces increased vascular permeability Antimicrobial peptides by macrophages Chemokines that recruit neutrophils The inflammatory complement fragments, C3a and C5a
Based on the data shown in chart, titled IL-2 Response by Macrophages that express TLR-XX would you predict that cytochalasin B treatment would inhibit TLR-XX dependent anti-viral immune responses to live RNA virus, Yes or No? Why? please be as concise as possible but clear in your response.
During inflammaion, host tissue may be damaged owing to the release of toxic oxygen derivatives produced by activated phagocytes. List some of hese toxic species and explain what cellular/biochemical mechanisms limit these damaging off-target effects.
An adaptive immune response underlying coeliac disease pathogenesis involves: a) Production of Th1 (T helper cell 1 type) cytokines that act to promote the production of antibodies to gluten peptides b) Production of anti-gliadin and anti-tissue transglutaminase antibodies via TH2 cytokines c) Conversion of glutamate to glutamine by deamination d) The early recognition of gluten peptides via pattern recognition receptors on epithelial cells and the subsequent release of Interleukin 15
The alternative pathway is an amplification loop for C3b formation that is accelerated by properdin in the presence of pathogens. The alternative pathway of complement activation has an important role in innate immunity, due to its ability to greatly amplify the amount of C3b deposited onto the pathogen surface. This amplification occurs because: The C3 convertase of the alternative pathway is much more active than those of the classical and lectin pathways. The C3 convertase of the alternative pathway works as a soluble enzyme in the plasma. The C3 convertase of the alternative pathway cannot be inactivated by complement regulatory factors in the host. The C3 convertase of the alternative pathway is more efficiently recruited to pathogen surfaces than the C3 convertases of the classical and lectin pathways. The C3 convertase of the alternative pathway contains C3b, and can generate more of itself.
Nearly all immune deficiency diseases that result in impaired TH17 and ILC3 function lead to chronic mucocutaneous candidiasis (CMC), usually accompanied by increased susceptibility to pyogenic bacterial infections. However, a subset of these patients also show increased susceptibility to intracellular bacterial infections, such as those caused by Mycobacteria species. What is the explanation for why some, but not all, of these patients have increased susceptibility to intracellular bacteria and which patients fall into this category?
The white blood cells known as T lymphocytes respond to antigens thatbind specifi cally to the T cell receptor, which consists of an antigen-binding αβ transmembrane protein as well as a set of transmembrane signaltransducing proteins known as CD3 that are targets of NRTKs. Thecytoplasmic domains of the CD3 proteins are positively charged and, in the absence of antigen, interact with the intracellular surface of the plasma membrane in such a way that buries several of their Tyr residues in the lipidbilayer. Antigen binding to the T cell receptor leads to a localized infl ux ofCa2+ ions. (a) Explain how a high concentration of Ca2+ could promote phosphorylation and activation of the CD3 proteins. (b) Would this henomenon make the T lymphocyte more or less responsive to the antigen?
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
Which of the following statements regarding TLR4 is false? (Select all that apply.) a. TLR4 is a Toll-like receptor expressed by macrophages, but not by NK cells. b. TLR4 is an example of a phagocytic receptor. c. TLR4 associates with CD14, which acts as a co-receptor to TLR4. d. The ligand for TLR4 is lipopolysaccharide (LPS). e. TLR4 is expressed as a homodimer on the cell surface. f. The extracellular domain of TLR4 associates with soluble MD2. g. TLR4 does not contain a cytoplasmic TIR domain.