When scientists added IL-17 to artery muscle cells in a dish, the cells started dying off in large numbers — especially at higher doses — which could explain how plaques get weak and burst.
Scientific Claim
In cultured murine vascular smooth muscle cells, exposure to 50 or 100 µg/mL of IL-17 for 48–72 hours increases apoptosis by 2–3 fold, as measured by annexin V staining and Hoechst nuclear condensation, suggesting IL-17 may directly weaken plaque stability by killing structural cells.
Original Statement
“The number of apoptotic cells (annexin V+ PI−) was markedly increased after treatment with 50 or 100 µg/ml IL-17A for 48 or 72 h... Cells treated with 50 or 100 µg/ml IL-17A for 48 or 72 h became shrunken and rounded, with condensed and broken nuclei.”
Evidence Quality Assessment
Claim Status
appropriately stated
Study Design Support
Design supports claim
Appropriate Language Strength
association
Can only show association/correlation
Assessment Explanation
The study shows a direct effect in isolated cells, but does not claim this mechanism occurs identically in vivo or in humans. The language appropriately reflects association and plausibility.
Evidence from Studies
Supporting (1)
The study found that a protein called IL-17 kills important cells in artery plaques, which can make the plaques more likely to break open — just like the claim says.