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,

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 14RE

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Concept explainers

Immunology

Immunology is the division of science involved with the immune reactions occurring in living organisms. The organisms are accustomed to evolving internal defense mechanisms to evade the invasion of microbial pathogens. Diverse cells are connected with stimulating the immune responses, which produce inhospitable conditions to the microbes prompting their lysis and thus inhibits the multiplication of the pathogens. The immune system can distinguish the pathogens through the aid of cellular intercommunication and launch responses to destroy them.

Question

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 functions

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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
IgM antibodies are much more efficient than IgG at activating the complement cascade. However, under certain circumstances, IgG antibodies will activate the complement pathway. One example of a situation in which IgG binding to its antigen will not trigger the complement cascade is when the IgG antibodies are neutralizing a bacterial toxin protein by blocking the receptor-attachment site on the toxin. the IgG antibodies are binding self-antigens, such as chromatin released from dead cells. the IgG antibodies bind to a bacterial surface by recognizing a repetitive polysaccharide component of the bacterial capsule. the IgG antibodies bind to a viral capsid protein that is present in more than 100 copies on the viral particle surface.
The 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.
Complement receptors and Fc receptors both contribute to removal of immune complexes from the circulation. Surprisingly, individuals with defects in the early components of the classical complement cascade (i.e., C1, C2, or C4) suffer from an autoimmune type of kidney damage, rather than from an immunodeficiency leading to increased susceptibility to infections. Why do these complement defects lead to autoimmune kidney damage?
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
Opsonization of pathogens by both antibodies and complement proteins (C3b) leads to uptake and destruction of the pathogen by phagocytic cells that express both Fc receptors and complement receptors. Which of the following in the figure below is the most efficient form of dual opsonization of the pathogen by antibody and C3b to maximize phagocytosis?
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Many cells in the human body have proteins on the surface that are able to interact with the receptors of helper T cells. Explain the mechanisms and why it is that such an interaction or signal does not usually result in an autoimmune reaction?