Underedited RNA sustains inflammation

This proposed study asks whether tissue cells can restart inflammation after stress has passed, and whether repairing that signal could prevent recurrence. The hypothesis centres on a cell's own double-stranded RNA, paired RNA strands that remain insufficiently edited after stress. MDA5, a sensor of this RNA, could trigger interferon, an antiviral signalling system, which then sustains the inflammatory RNA program. The test uses purified tissue cultures after immune-cell removal. If RNA destruction or active ADAR1, an RNA-editing enzyme, durably prevents recurrence while inactive ADAR1 does not, that pattern would support a cell-autonomous loop over explanations based on cell fusion, cell contacts or the surrounding matrix.