QUESTION 7 The importance of complement activation as an innate immune defense against infecti The evolution of complement avoidance strategies by many pathogens The existence of three different mechanisms for initiating complement activation The large number of proteins involved in the complement pathway O The large number of complement regulatory pathways expressed by the host
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- 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?Complement activation is a cascade reaction, with each component sequentiallyacting on others, in a similar way to the blood-clotting system. Discuss the effectsthat occur when peptides are generated from the activation by either the classicalor the alternative pathway. This is an immunology questionDiscuss the process an antigen presenting phagocyte [macrophages and dendritic cells] uses toidentify and move a target into the cell and its lysosomes – phagocytosis. Make sure you discussthe opsonins and their receptors.
- 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?It would be disastrous if a complement attack werenot confined to the surface of the pathogen that is the tar-get of the attack. Yet, the proteolytic cascade involved inthe attack liberates biologically active molecules at severalsteps: one that diffuses away and one that remains boundto the target surface. How does the complement reactionremain localized when active products leave the surface?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?
- Complement is an integral part of the innate immune response to bacteria . One of its mechanisms of action is to behave as an anaphylatoxin Describe the anaphylatoxic effects of complement identifying which components are activated.Multiple pathways for regulating complement activation limit the potential damage caused by complement deposition on host cells or caused by the spontaneous activation of complement proteins in the plasma. Genetic deficiencies in these mechanisms often lead to chronic inflammatory diseases, but in some cases can paradoxically lead to increased susceptibility to bacterial infections. This latter outcome may occur because: Complement regulatory proteins have dual functions in inhibiting and promoting complement activation. Uncontrolled complement activation leads to the depletion of serum complement proteins. The inhibition of the membrane attack complex by complement regulatory proteins normally leads to enhanced activation of the early steps of the complement pathway. Complement regulatory proteins normally cause the rapid depletion of plasma complement factors. Uncontrolled complement activation recruits the majority of phagocytic cells, leaving few remaining to fight infections in…On phagocytes and other cells, (?????) are receptors classified as part of the innate immune system that detect molecular motifs not usually found in humans, such as double stranded RNA or lipopolysaccharide and trigger an immune response.
- Mannose binding lectins (MBL) and ficolins are the two classes of proteins that can initiate the lectin pathway of complement activation. These proteins are selective for activating complement on the surfaces of microbial pathogens rather than host cells because: Their higher-order oligomeric structure can be assembled only after the monomers first bind to pathogen membranes. They only recruit MASP (MBL-associated serine proteases) proteins when bound to pathogen surfaces and not when bound to host cells. They only undergo the conformational change needed to activate MASP proteins when bound to a pathogen and not when bound to a host cell. They only bind to carbohydrate side chains and oligosaccharide modifications found on pathogen surfaces but not on host cell membranes. The activated MASP proteins are rapidly inactivated by hydrolysis when present on the surface of a host cell.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.Describe briefly the three effector functions of complement activation that result from the initial event of complement protein binding to peptidoglycans or LPS