Some primitive organisms, such as invertebrates, have no lymphocytes and thus lack an adaptive immune system, but they have somecomponents of an innate immune system, including phagocytes andcertain protective proteins. What are some general features of innateimmunity that make it very valuable to organisms lacking more specific antibody- and cell-mediated responses? What are some disadvantages to having only an innate immune system?

Some primitive organisms, such as invertebrates, have no lymphocytes and thus lack an adaptive immune system, but they have somecomponents of an innate immune system, including phagocytes andcertain protective proteins. What are some general features of innateimmunity that make it very valuable to organisms lacking more specific antibody- and cell-mediated responses? What are some disadvantages to having only an innate immune system?

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 6QP

See similar textbooks

Similar questions

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.
Why is it necessary for immature T lymphocytes toundergo a two-step selection process through whichantigen-reactive cells are first selected followed bythe elimination of cells that react strongly withself-antigens?
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.
At first glance, it would seem a dangerous strategyfor the thymus to actively promote the survival, matura-tion, and emigration of developing T cells that bind weaklyto self peptides bound to self MHC molecules. Would itnot be safer to get rid of these T cells, along with those thatbind strongly to such self-peptide–MHC complexes, as thiswould seem a more secure way to avoid autoimmune reac-tions?
How do cytokine barrier provide innate immunity in human ?
In general, what are consequences of activation of the TH1 arm of the immune response? Activation of the TH2 arm?
What is the relationship and differences between receptor-mediated endocytosis and TLR in relation to innate immunity?
Helper T cells are affected by HIV, how come is this receptor key to the immune system? which line of defense are we referring to? How is it connected to the immune system and which line of defense? Hence, based on your prompt, how are cytokines linked to the defense mechanism of HIV virus? Do you know or can you explain the cascade of events dealing with PAMPS, TLRs, interferon? What do they have to do with the second line of defense?
Immunity can be of many types: natural activeimmunity, natural passive immunity, artificial activeimmunity and artificial passive immunity. Which of theseforms of immunity confer immune memory?
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?
Inflammation is the hallmark of an activated immune response. Explain how inflammation is triggered by both innate and adaptive immune mechanisms. Are the inflammatory cells the same for both methods of activation? Why does inflammation subside as an infection is controlled?
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?