EBK LIFE: THE SCIENCE OF BIOLOGY
11th Edition
ISBN: 8220103935432
Author: Sadava
Publisher: MAC HIGHER
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Chapter 41.1, Problem 2R
Summary Introduction
To review:
The
Introduction:
TLRs are a class of receptors involved in providing innate immunity. TLRs recognize a specific molecule or pattern called pathogen-associated molecular pattern (PAMP), which is present in many pathogens.
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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 major cause of septic shock is the presence of lipopolysaccharide (LPS) from bacteria in the blood. suppose you have available purified LPS and several strain of mice, each with a mutation that inactivates a particular TLR gene. How might you use these mice to test the feasibility of treating septic shock with a drug that blocks TLR signaling?arrow_forwardThe 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?arrow_forwardThe small fragments of some complement proteins initiate a local inflammatory response. Recent studies using mouse models of pulmonary inflammation (a model for human asthma) have found that mice deficient in the C3a receptor have greatly reduced disease symptoms when challenged with inhaled preparations containing extracts of the fungal pathogen Aspergillus fumigatus. Specifically, the C3a receptor-deficient mice showed reduced influx of granulocytes and lymphocytes into the lung and reduced fluid in the lung after challenge. What is the explanation for these findings?arrow_forward
- Some primitive organisms, such as invertebrates, have no lymphocytes and thus lack an adaptive immune system, but they have somecomponents of an innate immune system, including phagocytes andcertain protective proteins. What are some general features of innateimmunity that make it very valuable to organisms lacking more specific antibody- and cell-mediated responses? What are some disadvantages to having only an innate immune system?arrow_forwardSome viruses have mechanisms to down-regulate MHC class I protein expression on the surface of cells in which the virus is replicating. This immune evasion strategy might prevent effector CD8 cytotoxic T cells from recognizing and killing the virus-infected cells. Would this immune evasion strategy also prevent the initial activation of virus-specific CD8 T cells? Yes, because no viral peptide:MHC class I complexes would form to activate CD8 T cells. No, because dendritic cells would take up infected cells and cross-present viral peptides to activate CD8 T cells. No, because some presentation of MHC class I complexes with viral peptides would occur before the virus could down-regulate all the surface MHC class I protein. Yes, because this immune evasion strategy would also function in dendritic cells, even if the virus doesn’t replicate in dendritic cells. No, because the type I interferon response induced by the virus infection will up-regulate MHC class I expression and override the…arrow_forwardTLRs activate NFkB, AP-1, and IRF transcription factors to induce the expression of inflammatory cytokines and type I interferons. A key feature of TLR signaling is the ability to induce inflammatory cytokine gene expression extremely rapidly following TLR stimulation. This is accomplished by signaling pathways using several mechanisms to activate transcription factors that are already present in the cell prior to TLR stimulation, but are kept in an inactive state. These signaling pathways use all of the following mechanisms EXCEPT: Induced ubiquitination leading to protein degradation Induced ubiquitination inducing protein–protein interactions Induced phosphorylation leading to nuclear translocation Induced phosphorylation leading to kinase activation Induced phosphorylation preventing protein degradationarrow_forward
- Which proteins involved in the activation of T cells have the capacity for transduction without the need to be activated by a family of kinases?arrow_forwardVirus 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…arrow_forwardTumor necrosis factor alpha (TNF-α) is an important cytokine used by immune cells to initiate and coordinate inflammatory responses. Inflammation is a key response to cell damage or infection, but can, in some diseases, spiral out of control and become more of a problem than the original cause (COVID-19 lung damage is a relevant example...). TNF-α receptors exist on many cell types. Let’s study the interaction between TNF-α (T) and its receptor (R), to form an activated complex C: T + R ↔ C A macrophage is measured to have ~105 TNF-α receptors on its surface. If the macrophage is immersed in a high concentration of TNF-α molecules (i.e. L0 ≅ L), how will the number of activated receptors change over time? Plot this trend for the case L0 =10 nM, kf=106 M-1 min-1, kr=0.1 min-1. There is constant ligand concentration and an initial condition of C0 = 0. We are given the constants needed to model the number of activated receptors over time and can use the following equation:arrow_forward
- 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 complementarrow_forwardWhy are the mannose-binding lectin and alternative pathwaysconsidered part of the innate immune system?arrow_forwardIn some viral infections, interferons, which are hydrophilic, are secreted by some white blood cells. These bind nearby cells causing uninfected cells to produce protective antiviral proteins. Based on this information, what type of signaling molecule are interferons? - Autocrine - Hormonal - Neural - Paracrine - Neurohormonearrow_forward
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