The innate immune system has to be able to detect foreign invaders. Explain two ways that the innate immune system is able to detect these foreign invaders to allow a response to be mounted.
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The innate immune system has to be able to detect foreign invaders. Explain two ways that the innate immune system is able to detect these foreign invaders to allow a response to be mounted.
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- Toll-like receptors represent an ancient pathogen-recognition system. The first pattern recognition receptor (PRR) important in innate immune responses was discovered in the fruit fly Drosophila melanogaster. Stimulation of this receptor, called Toll, induces: The synthesis of prostaglandins and leukotrienes The inflammatory response in Drosophila hemolymph vessels The production of antimicrobial peptides The recruitment of phagocytic cells to the site of infection The activation of Drosophila complementNeutralizing 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 0The 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 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.1) According to the video, what is another name for the innate immune sys and what does this system do? 2) According to the video, what causes inflammation and what cells cause it? 3) According to the video, what happens to neutrophils after they consume a pathogen? 4) According to the video, natural killer cells; what do they do? 5) The adaptive/acquired immune system can tell the difference between types of pathogens: true or false? 6) According to the video, helper t- function: 7) According to the video, cytotoxic t cells function: 8) According to the video, memory cells function: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
- 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.picture 1 shows the directed migration of two immune cell types, neutrophils (red) and macrophages (green) to a laser-induced injury in the ear of a mouse. As you can observe from the video, there are three stages to this process: 1) an initial phase characterized by fast recruitment of neutrophils (red) to the site of injury followed by 2) the slower recruitment of macrophages after which 3) the interaction between both cell types is stabilized. Recruitment to the injury site is mediated by leukotriene B4 (LTB4), a potent immune signaling molecule (Figure 1A). LTB4 binds to BLT1, a G-protein coupled receptor (GPCR), activating various signaling pathways and resulting in immune cell migration to the site of injury (Figure 1B). With this background information and your knowledge of cell and molecular biology, describe in detail in your own words, as many molecular processes as you can identify that must take place for the cell migration process depicted in the video to be achieved. For…What part of defense would likely be affected if the pathogen contained a mutation in it's pathogen-associated molecular patterns (PAMPs)? the pathogen would secrete greater amounts of toxins. the pathogen might not be recognized by the host. the pathogen would be easily recognized by the host's TLRs. the pathogen would not be able to penetrate the host's physical barriers.
- For some time there has been evidence that the Bacille Calmette-Guérin (BCG) vaccine provides protection not only against the target disease (Mycobacterium tuberculosis), but also enhances responses to other infections (such as Staphylococcus aureus and Candida albicans). Do you think the enhanced response to other infections, as described, is due to innate responses to the vaccine or adaptive responses? Explain your answer.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?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.