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The PAMP recognized by TLR3 is doublestranded RNA (dsRNA). Against which pathogens would TLR3 be an effective immune receptor?
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- 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?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 complementSome 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…
- 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 C5aThe 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?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?
- Some Pattern Recognition Receptors (PRRs) recognize nucleic acids, like RNA or DNA. Since our own cells contain human RNA and DNA, the activation of innate immune pathways by these PRRs must rely on additional criteria to discriminate self from nonself. Additional criteria include everything EXCEPT: The subcellular location of the RNA The presence of adenosine residues in viral RNA The methylation state of the DNA Unique structures found on viral RNA The subcellular location of the DNAIn Type II innate bacterial immunity, which of the following molecules are required for proper assembly and targeting of the Cas9 protein? MRNA TRNA miRNA SİRNA O crRNA/tracrRNAInfluenza virus causes serious disease and death, and is responsible for one of the largest pandemics in recorded history. However, the process by which antigens are made and processed are not unique to that virus. Answer the following questions to trace how infected cells will become recognizable by the TCR of a compatible T-cell. A) Where are the viral proteins made? B) Describe the process by which viral proteins are broken down into peptides. Be sure to discuss any unique molecules or organelles that participate in the process. C) Which MHC molecule presents these peptides? D) Now that you have made peptides from the viral antigen, how do they get to and bind to the MHC molecule? Describe the process. What unique molecules are involved in this process? E) What is the final destination for these molecules/epitopes, and how do they reach that destination?
- Describe the signal transduction pathway that is activated when LPS binds to TLR-4.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?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