Harms, MikeBrown, Corinthia2024-08-302024-08-302024https://hdl.handle.net/1794/29890Inflammation is a vital process our bodies use to remove foreign entities and help restore function to damaged tissue. However, when inflammation excessively activates it can lead to arthritis, neurodegeneration, and sepsis, which contributes to 11 million deaths a year. Inflammation results from inflammatory cytokines produced by the NF-kB pathway, activated by Toll-Like Receptor 4 (TLR4). We know that certain lipopolysaccharides (LPS) present on gram-negative bacteria drive the dimerization of TLR4 and activate inflammatory cytokine production. However, we do not completely understand the rules which govern TLR4 activation, making it difficult to control this regulator of inflammation, particularly in clinical applications.en-USCC BY 4.0TLR4Helix ShiftingProtein EvolutionInternal Signaling MismatchProtein CassetteThesis/Dissertation0009-0002-0920-6884