TLR-4 recognizes bacterial lipopolysaccharide in association with the host accessory proteins MD-2 and CD14. True/False: All mammalian TLRs have been shown to directly bind to microbial products, leading to TLR signaling.
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TLR-4 recognizes bacterial lipopolysaccharide in association with the host accessory proteins MD-2 and CD14. True/False: All mammalian TLRs have been shown to directly bind to microbial products, leading to TLR signaling.
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- 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 C5aWhich of the following apply to the specific function of IL-2? OIL-2 promotes vasodilation and vascular permeability OIL-2 promotes rapid mitosis by lymphocytes IL-2 promotes the perforation of the plasma membrane of host cells infected with an intracellular pathogen O None of the statements apply OIL-2 promotes complement-directed lysis of the pathogen OIL-2 promotes feverWhy is it significant that toll-like receptors (TLRs) are found on both the plasma membrane and internal cell membranes?
- True/False: Antibody binding to a pathogen surface is greatly enhanced when both antigen-binding sites of the antibody are engaged at once, a feature known as bivalent binding. It is possible for antibodies to bind bivalently to a wide variety of components on many different pathogen surfaces due to the flexibility in the protein at the hinge region and at the V–C junction.True/False: Several pathogens produce proteins, either membrane-bound or secreted, that inactivate C3b that might be deposited on the pathogen surface. C3b is specifically targeted due to its central position in all three complement pathways. Explain.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?
- The formation of the C3 convertase is a key step in complement activation that occurs in all three complement pathways. This enzyme cleaves C3 in blood plasma, leading to a conformational change in the C3b fragment that exposes its reactive thioester group. The activated C3b is potentially harmful to the host, if it becomes covalently attached to a host cell, rather than to the surface of a pathogen. This deleterious outcome is largely avoided by: The inability of active C3b to diffuse away in the blood plasma. The inability of active C3b to covalently attach to the membranes of eukaryotic cells. The rapid hydrolysis of active C3b in solution, rendering it inactive. The tight binding of active C3b to the C3 convertase. The ability of active C3b to recruit phagocytic cells.B cells express a complement receptor that binds to C3b cleavage products, such as iC3b and C3dg. When a B cell with an antigen receptor that specifically recognizes that pathogen also has its complement receptor stimulated because the pathogen is opsonized with these C3 fragments, B cell activation is greatly enhanced. Due to this mechanism, B cells can be activated by much lower concentrations of antigen (in this case, the pathogen) than if the antigen is devoid of complement components. This mechanism functions to: Ensure that pathogens are readily detected by the adaptive immune system before they replicate to high levels in the host Prevent B cells from being activated in response to antigens that are not pathogens Allow B cells to phagocytose the pathogen and help destroy it Induce increased rounds of B cell replication to make more pathogen-specific B cells Allow the B cell to block pathogen replication by interfering with multiple pathogen surface functionsThe 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.
- True or False: In non-disseminated infections, Mycobacterium species are restrained by type-1 responses which increase macrophage phagocytic activity, NK and T cell activation. True or False: The low-affinity Fcε receptor (FcεRII/CD23) on mast cells will bind to IgE in tissues in the absence of antigen.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.Antibodies can have multiple mechanisms of action. The main mechanism is "flagging" a foreign body for phagocytosis and degradation. Another mechanism is... Select one: a. Binding of the Fc domain to T cells for cooperative antigen recognition and destruction. b. Altering the local pH by the formation of carbamate upon reaction with CO2 to denature protein antigens. c. Binding of the variable region to multiple different/distinct sites on the antigen. d. None of these. e. Binding of the antigen in regions essential for its function.