Which of the following is specific to the immediate events of innateimmune system inflammation?O Diapedesis of neutrophils into the tissuesCytokine secretion by macrophage andNendritic cellsVasodilation, vascular permeability, and cell adhesion molecule (CAM) expressionO Secretion of IL-2None of the statements are characteristic of immediate events of inflammation Gram negative cell walls contain lipopolysaccharide (LPS) as a uniquecomponent. All of the following apply to LPS EXCEPTO LPS is composed of mycolic acids that protect the cell from phagocytosisLPS is a PAMP that can be recognized by toll-like receptors (TLRS) as a foreignmolecule fo rphagocytosisO LPS can be a target for specific IgG for ADCC-opsonizationLPS can be recognized by B cells in the aosence of MHC moleculesAll of the answers apply, no exceptionO LPS is found in the outer membrane of Gram negative cells

Innate immunity is the immune response that consist of all defence elements with which an…

Which of the following is specific to the immediate events of innate immune system inflammation? Diapedesis of neutrophils into the tissues O Cytokine secretion by macrophage and Nendritic cells O Vasodilation, vascular permeability, and cell adhesion molecule (CAM) expression O Secretion of IL-2 None of the statements are characteristic of immediate events of inflammation

Which of the following is specific to the immediate events of innate immune system inflammation? Diapedesis of neutrophils into the tissues O Cytokine secretion by macrophage and Nendritic cells O Vasodilation, vascular permeability, and cell adhesion molecule (CAM) expression O Secretion of IL-2 None of the statements are characteristic of immediate events of inflammation

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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G-protein-coupled receptors on phagocytes link microbe recognition with increased efficiency of intracellular killing. The NBT (Nitro Blue Tetrazolium) test is used to diagnose the genetic disorder Chronic Granulomatous Disease (CGD). To perform this test, peripheral blood cells from the patient are stimulated with bacterial extracts, and then incubated with the NBT compound. Normal neutrophils turn blue in this test due to cleavage of the compound, while patient neutrophils remain uncolored, as shown in Figure below. Name a neutrophil receptor that is likely to be stimulated by the bacterial extract in this assay, and describe how this receptor regulates the activity of the enzyme that cleaves NBT.
Mycobacteria are intracellular pathogens that have adapted to life inside phagocytic cells, such as macrophages. These intracellular bacteria are taken up by phagocytosis, similar to other pathogens, but the bacteria are not killed. One possible mechanism that could account for this immune evasion by mycobacteria is their ability to: Prevent induction of nitric oxide production in the phagosome Prevent the acidification of phagosomes Prevent the expression of antimicrobial peptides in the phagosome Prevent fusion of phagosomes with lysosomes Kill the macrophage before it kills them
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?
TH2 cells coordinate type 2 responses to expel intestinal helminths and repair tissue injury. The immune response to helminthic worm infections in the gastrointestinal tract requires specialized mechanisms due to the fact that helminths are too large to be ingested and destroyed by phagocytes. For example, cytokines made by TH2 cells elicit responses from multiple non-hematopoietic cell types that aid in parasite expulsion. Name two of these cell types and for each of them, their response to TH2-produced cytokines.
The terminal complement proteins polymerize to form pores in membranes that can kill certain pathogens. The terminal components of the complement pathway assemble to form a membrane attack complex that can induce pathogen lysis and death. Yet, evidence indicates that this feature of complement is less important than the earlier steps that promote pathogen opsonization and induce inflammation. This conclusion is based on: In vitro experiments showing that very few species of bacteria are susceptible to lysis by the membrane attack complex Experiments indicating that only bacteria, but not viruses or fungi, are susceptible to lysis by the membrane attack complex The very low levels of terminal complement components in the serum The fact that other mammalian species lack the terminal components of the complement pathway needed to form the membrane attack complex The limited susceptibility to infections of patients with deficiencies in terminal complement components
In addition to phagocytosis, neutrophils use a process called NETs. Which one of the following describes this process? Group of answer choices A. NETs is a neutrophil process that activates the complement system of proteins, which destroys pathogens. B. A net-like structure of DNA, histones, lactoferrins, gelatinase, cathepsin G, and myeloperoxidase is secreted at pathogens. Together these chemicals destroy pathogens. C. NETs works when neutrophils secrete major basic proteins onto pathogens, destroying the pathogens' cell membranes. D. NETs are chemicals secreted by neutrophils that trigger the rapid maturation of lymphoid stem cells into lymphocytes.
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
Although the complement cascade can be initiated by antibodies bound to the surface of a pathogen, complement activation is generally considered to be an innate immune response. This is because: Two of the three pathways for complement activation are initiated by constitutively produced recognition molecules that directly interact with microbial surfaces. When the complement cascade leads to the formation of a membrane-attack complex, the pathogen is killed. Several of the soluble products generated by complement activation lead promote the inflammatory response. Complement proteins bound to the pathogen promote uptake and destruction by phagocytic cells. The C3 convertase is only produced when complement activation is initiated by antibody binding to a pathogen.
Which of the following would you anticipate would be secreted through the Type III secretion system during infection? a secondary messenger effector that is unable to cross the host cell membrane, such as the AexT protein that disrupts the host cell cytoskeleton the superantigen TSST that is responsible for the signs and symptoms associated with toxic shock syndrome a pore-forming cytolytic toxin, such as a hemolysin not enough information to determine the AB toxin responsible for the flaccid paralysis associated with botulism
What is not true regarding drug delivery uptake? Most nanoparticles enter cells through endocytosis Cells are not able to internalize particles of nanoscale Nanoparticles can be used to deliver high drug doses to cell Nanoparticles can enter the cell via phagocytosis What is not true regarding the foreign body response? First, proteins form the blood and interstitial fluid adsorb to surfaces of the implant. Recruitment of cells comes in, mainly macrophages and neutrophils. With time the material, proteins, and cells get fused. Encapsulation of the foreign material occurs immediately after implantation When thinking about measurement systems, which is correct? The processor detects the input. The sensor can amplify or filter the signal. The input is the end product the user will know. The receiver presents a message that is interpretable.
Virus infections induce production of interferons that act on infected cells to enhance their recognition by CD8 cytotoxic T cells. To counter these mechanisms, viruses often encode proteins that interfere with antigen processing and presentation. In an experiment, cells infected with Virus X are treated with interferon and compared with uninfected cells treated with interferon. Proteasomes are isolated from the two cell populations and their enzymatic activities are compared. The data in figure below show the amino acid preferences for cleavage of peptides by the two samples of proteasomes. Based on these data, Virus X most likely encodes a protein that interferes with: The expression of MHC class I on the surface of the infected cell The rate at which peptides are produced from intact proteins in the infected cell The transport of peptides from the cytosol to the endoplasmic reticulum in the infected cell The replacement of constitutive proteasome subunits with immunoproteasome…
Some pathogenic microorganisms encode proteins, such as the Staphylococcus Protein A, that bind to immunoglobulin constant region domains with high affinity. These microbial proteins provide a benefit to the microorganism by: Preventing antibodies bound to the microbe from binding to Fc receptors on phagocytes Blocking the binding of anti-microbial antibodies to the pathogen surface Cleaving the antibody into fragments that separate the antigen-binding region from the effector function Inducing aggregation of the anti-microbial antibodies by multivalent binding to the pathogen-derived protein Preventing the antibody from neutralizing the pathogen