Tumor Necrosis Factor (TNF) Receptors in Psoriasis
Date of Award
Dr. Erin Johnson
Psoriasis is an autoimmune disorder in which overactive keratinocytes trigger the inflammatory response, leading to red and painful skin. The inflammatory response is triggered when TNF-α binds to either of its two receptors, p55 or p75, and induces expression of leukocyte adhesion molecules on endothelial cells. Inflammation is triggered when these endothelial cell expressed molecules interact with leukocytes in the blood. Using a psoriasis model organism, the imiquimod (IMQ) treated mouse, it was previously found that knocking out the p75 receptor is sufficient to reduce inflammation. This study used qPCR to analyze RNA levels and determine the underlying causes for the phenotypic differences between p55, p75, and double knockout IMQ-treated mice. It was found that the double knockouts were equally or more successful at reducing the expression of the pro-inflammatory genes E-selectin, ICAM-1, P-selectin, VCAM-1, PECAM-1, and PRMT5 from wildtype mouse levels as compared to single knockout mice.
Lee, MacKenzie, "Tumor Necrosis Factor (TNF) Receptors in Psoriasis" (2016). Senior Honors Projects. 95.
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