Experimental Mouse Model And Its Effect On Normal Immune System Essay

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The article that inspired this research proposal described the use of engineered human embryonic kidney cells, coated in a porous algal sheath, in the selective mediation of psoriatic inflammation in an experimental mouse model. The engineered converter cells were able to detect the presence of psoriasis related pro-inflammatory markers TNF (tumor necrosis factor) and IL-22 (an interleukin) in combination, through linked receptors (Di Domizio and Gillet 2015). TNF receptor signals first activate IL-22 receptors (IL-22R), which in turn switches a signal transducer and activator of transcription 3 (STAT3) on. The STAT3 responsive promoter finally drives the manifestation of anti-inflammatory cytokines IL-4 and IL-10 (Di Domizio and Gillet 2015). This study concluded that converter cell activity can be tuned to specific inflammation markers without affecting normal immune system response to pathogens (Di Domizio and Gillet 2015). While there are still far too many hurdles to bring this study to human trial, it did highlight the potential treatment of any number of chronic inflammatory conditions. It is therefore logical to apply this reasoning to the chronic inflammatory autoimmune condition of rheumatoid arthritis. Can engineered converter cells be designed to prevent synovial joint damage from induced rheumatoid arthritis synovial joint damage in a mouse model experiment?
Hypothesis and Prediction
Treatment with engineered converter cells that have been tuned to detect and

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