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- 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.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?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?
- Based on your understanding of the innate immune system list 3 broad categories (and AT LEAST ONE specific example in each category) that constitute the first line of defense mechanisms by the innate immune system. (Give an approximate time line for this type of defense) If this defense system is breached describe the process that follows (second line of innate defense). Explain how pathogens are detected and dealt with at this time with specific pathogen groups in mind, innate immune cells and molecular components involved. (Give an approximate timeline for this response) What are the TWO possible outcomes of this response and the way forward?Where are major histocompatibility complex-I (MHC-I) molecules located in the human body (cells)? Briefly describe how these surface markers present antigens to other cells. (Make sure to include where the antigen originates and what type of T-cell interacts with MHC-I antigen presentation.)Two BMI2607 students are studying for the May/June exam, when they reach a learning unit on the body’s defensive systems. One of them insists that complement is part of the nonspecific second line of defense, but the partner insists that complement is part of an antibody immune response in the third line of defense. As the third person to join them, discuss how would you explain to them that they are both correct?
- 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?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 functionsWhich of the following is not true about the complementsystem?(a) It is a set of more than 20 proteins that play a key rolein host defense by specifically acting in different waystoward different microorganisms.(b) Its general functions include enhancing phagocytosis byphagocytes, lysing microbes and enveloped viruses directly, and generating peptide fragments that regulateinflammation and immune responses.(c) It is a fast-acting innate host defense that works in a cascade.(d) There are three pathways classical, lectin, and alternative.(e) The effects of each activation pathways are the same.
- Which of the following statements is NOT correct? Group of answer choices -Natural killer cells are cytolytic lymphocytes that mediate ADCC -Neutrophils carry out phagocytosis of C3b-tagged particles -Macrophages carry out phagocytosis of C3b-tagged particles -Mast cells produce granules containing the cytotoxin perforin -B lymphocytes express a receptor for complement proteinsAt 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?What is the relationship and differences between receptor-mediated endocytosis and TLR in relation to innate immunity?