Human immune system During the inflammatory response, histamine plays a key role in causing capillaries to become more permeable to phagocytic cells such as neutrophils. Antibodies directly kill bacterial cells by activating cell death programs that lead to apoptosis. Interferons are signaling molecules produced by bacteria that block (or interfere) with the ability of plasma cells to release antibodies.

Human immune system During the inflammatory response, histamine plays a key role in causing capillaries to become more permeable to phagocytic cells such as neutrophils. Antibodies directly kill bacterial cells by activating cell death programs that lead to apoptosis. Interferons are signaling molecules produced by bacteria that block (or interfere) with the ability of plasma cells to release antibodies.

Human Heredity: Principles and Issues (MindTap Course List)

11th Edition

ISBN:9781305251052

Author:Michael Cummings

Publisher:Michael Cummings

Chapter17: Genes And The Immune System

Section: Chapter Questions

Problem 2QP: The Complement System Kills Microorganisms The complement system supplements the inflammatory...

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It is often helpful to draw a complicated pathway in the form of a flow chart to visualize the multiple steps and the ways in which the steps are connected to each other. Draw the antibody-mediated immune response pathway that acts in response to an invading virus.
The Adaptive Immune Response Is a Specific Defense Against Infection Name the class of molecules that includes antibodies, and name the five groups that make up this class.
The Adaptive Immune Response Is a Specific Defense Against Infection Identify the components of cellular immunity, and define their roles in the immune response.
Complement proteins function in defense by _______. a. neutralizing toxins b. enhancing resident bacteria c. promoting inflammation d. forming pores that cause pathogens to disintegrate e. both a and b f. both c and d
The Complement System Kills Microorganisms The complement system supplements the inflammatory response by directly killing microorganisms. Describe the life cycle of complement proteins, from their synthesis in the liver to their activity at the site of an infection.
Neutralizing antibodies are effective at preventing infection or toxicity mediated by pathogens or their toxic products. In fact, nearly all vaccines currently in use function by eliciting neutralizing antibodies. One example is the tetanus vaccine, in which neutralizing antibodies are generated against an inactivated form of the tetanus toxin (the tetanus toxoid). The most important feature of a neutralizing antibody is having high affinity for the antigen. being efficient at activating the complement cascade. having a high degree of multivalency, such as being a pentamer or hexamer of immunoglobulin monomers. being present at a high concentration in the circulation. 0 0 0 0
Individuals infected with herpes simplex virus (HSV) mount protective antibody responses directed against surface glycoproteins of the virus. These antibodies are critical to viral clearance. The act to neutralise any virus trying to infect a person’s cells as well as activating the classical pathway of complement and cytotoxic cell-mediated killing of infected target cells. Having a deficiency in the complement component C3 greatly impairs a person’s ability to control HSV infections. To understand this further, you will investigate this in the lab. Using C3-deficient mice, you infect them with HSV at day 0 and then a second time 4 weeks later. A hypothesis is a tentative answer to a scientific question and is an important part of practical experiments. A testable hypothesis is statement that can be proved or disproved as a result of experimentation. Q1. State the problem that you are trying to solve. And then formulate a robust testable hypothesis for your…
Individuals infected with herpes simplex virus (HSV) mount protective antibody responses directed against surface glycoproteins of the virus. These antibodies are critical to viral clearance. The act to neutralise any virus trying to infect a person’s cells as well as activating the classical pathway of complement and cytotoxic cell-mediated killing of infected target cells. Having a deficiency in the complement component C3 greatly impairs a person’s ability to control HSV infections. To understand this further, you will investigate this in the lab. Using C3-deficient mice, you infect them with HSV at day 0 and then a second time 4 weeks later. A hypothesis is a tentative answer to a scientific question and is an important part of practical experiments. A testable hypothesis is statement that can be proved or disproved as a result of experimentation. You perform an ELISA to measure the antibody response of the C3-deficient and normal mice (referred to as wild-type – WT)…
The mechanism of cross-presentation by dendritic cells is an essential pathway for generating CD8 T cell responses to some intracellular pathogens. If this pathway did not exist, we would be highly susceptible to: Intracellular pathogens that can survive inside macrophage endocytic vesicles Intracellular pathogens that are able to evade antibody responses Intracellular pathogens that do not infect and replicate in dendritic cells Intracellular pathogens that can spread from cell to cell by inducing cell fusion Intracellular pathogens that infect and replicate in red blood cells
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
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.
Ingestion of complement-tagged pathogens by phagocytes is mediated by receptors for the bound complement proteins. Even when the complement cascade fails to proceed beyond generating the C3 convertase, complement activation is effective at inducing pathogen uptake and destruction. This process of immune protection is mediated by: Activation of complement inhibitory receptors on phagocytes that promote pathogen uptake Activation of soluble proteases in the serum that disrupt pathogen membranes Engagement of complement receptors on phagocytes by C3b and its cleavage products which promotes phagocytosis Engagement of complement receptors on B cells that promotes antibody production Stimulation of antimicrobial peptide secretion by phagocytes

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	During the inflammatory response, histamine plays a key role in causing capillaries to become more permeable to phagocytic cells such as neutrophils.
	Antibodies directly kill bacterial cells by activating cell death programs that lead to apoptosis.
	Interferons are signaling molecules produced by bacteria that block (or interfere) with the ability of plasma cells to release antibodies.