1.Explain the link between these factors and the symptoms seen in IRIS (you’ve been given all the information on IRIS you need). In other words, how are the following contributing to the symptoms we see in IRIS: TLR signalling, higher amount of DAMPs, greater number of activated monocytes, and increased C1q:C1-inhibitor ratio.2.Review the innate information provided earlier; could the innate components implicated in IRIS (the four factors) act in coordination with the adaptive immune system? In other words, are there ways the innate components discussed could directly or indirectly influence the adaptive response? Why or why not? 3.How can TLR4 and MyD88 contribute to the inflammation, ROS production, and/or NF-kB and AP-1 activation, found in IRI? (Note: you may decide TLR4 and MyD88 contribute in the same way, or in different ways; you may decide that they contribute only to one factor like ROS, but not another, or all of them)Why would knocking out MyD88 have a greater effect than knocking out just TLR4?Why is there increased injury when MyD88 is only expressed in myeloid lineage cells when compared to when MyD88 is only expressed in non-myeloid lineage cells?
4.Explain how C5 and neutrophils can contribute to the inflammation, ROS production, and/or NF-kB and AP-1 activation, found in IRI. (Note: you may decide C5 and neutrophils contribute in the same way, or in different ways; you may decide that they contribute only to one factor like ROS, but not NF-kB, or to both)
5.Do the results from the Aslan lab support the results found by the Shantsila lab? Why or Why not? (think, do they both overlap with a common process, cell type, or such?)6. A. What pathway/response is targeted by both Hepatitis C and the Flaviviruses? Why would targeting this component/response be useful to the virus?
6B. What pathway/response is targeted by both EBV and Adenovirus? Why would targeting this component/response be useful to the virus?
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