The effector mechanisms that are recruited to clear an infection depend on the infectious agent. In addition to producing distinct innate responses locally at the site of infection, the different cytokines produced during type I, type 2, or type 3 immune responses also induce distinct adaptive immune responses that are tailored to the eradication of the three different classes of pathogens. One example is the production of different classes of antibodies during type I, type 2, or type 3 responses. Which step during the induction of the adaptive immune response is the key to generating and coordinating the three different immune modules?

The effector mechanisms that are recruited to clear an infection depend on the infectious agent. In addition to producing distinct innate responses locally at the site of infection, the different cytokines produced during type I, type 2, or type 3 immune responses also induce distinct adaptive immune responses that are tailored to the eradication of the three different classes of pathogens. One example is the production of different classes of antibodies during type I, type 2, or type 3 responses. Which step during the induction of the adaptive immune response is the key to generating and coordinating the three different immune modules?

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 15RE

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Although the complement cascade can be initiated by antibodies bound to the surface of a pathogen, complement activation is generally considered to be an innate immune response. This is because: Two of the three pathways for complement activation are initiated by constitutively produced recognition molecules that directly interact with microbial surfaces. When the complement cascade leads to the formation of a membrane-attack complex, the pathogen is killed. Several of the soluble products generated by complement activation lead promote the inflammatory response. Complement proteins bound to the pathogen promote uptake and destruction by phagocytic cells. The C3 convertase is only produced when complement activation is initiated by antibody binding to a pathogen.
The classical complement pathway is initiated by C1q binding to the surface of a pathogen. In some cases, C1q can directly bind the pathogen, for instance by recognizing proteins of bacterial cell walls, but in most cases C1q binds to IgM antibodies that are bound to the pathogen surface. How does this IgM-binding feature of C1q contribute to rapid, innate immune responses rather than to slow, adaptive responses? C1q induces B lymphocytes to begin secreting antibody within hours of pathogen exposure. Natural antibody that binds to many microbial pathogens is produced prior to pathogen exposure. C1q binds to C-reactive protein which then binds to IgM on the pathogen surface. C1q directly induces inflammation, recruiting phagocytes and antibodies from the blood into the infected tissue. C1q binds to dendritic cells in the infected tissue, inducing them to secrete inflammatory cytokines.
Which of the following is NOT an example of non-specific (innate) resistance mechanisms interacting directly with specific acquired immunity mechanisms? what option below is the answer? Antibodies binding to bacterial surface antigens, coating (opsonizing) the bacteria and enhancing their phagocytosis by leukocytes Macrophages and dendritic cells presenting antigens to lymphocytes None of the other four answers (All are examples of interaction between innate and acquired resistance) Antibody-dependent cell-mediated cytotoxicity Complement being activated by antigen-antibody binding
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